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  4.    <title>movement disorders</title>
  5.    <link>https://pubmed.ncbi.nlm.nih.gov/rss-feed/?feed_id=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;utm_medium=rss&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;v=2.18.0.post9+e462414&amp;utm_source=Feedvalidator&amp;ff=20240501180032</link>
  6.    <description>movement disorders: Latest results from PubMed</description>
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  11.    <lastBuildDate>Wed, 01 May 2024 22:00:33 +0000</lastBuildDate>
  12.    <pubDate>Wed, 01 May 2024 06:00:00 -0400</pubDate>
  13.    <ttl>120</ttl>
  14.    <item>
  15.      <title>Functional implications of NHR-210 enrichment in C. elegans cephalic sheath glia: insights into metabolic and mitochondrial disruptions in Parkinson's disease models</title>
  16.      <link>https://pubmed.ncbi.nlm.nih.gov/38691171/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  17.      <description>Glial cells constitute nearly half of the mammalian nervous system's cellular composition. The glia in C. elegans perform majority of tasks comparable to those conducted by their mammalian equivalents. The cephalic sheath (CEPsh) glia, which are known to be the counterparts of mammalian astrocytes, are enriched with two nuclear hormone receptors (NHRs)-NHR-210 and NHR-231. This unique enrichment makes the CEPsh glia and these NHRs intriguing subjects of study concerning neuronal health. We...</description>
  18.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Mol Life Sci. 2024 May 1;81(1):202. doi: 10.1007/s00018-024-05179-2.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Glial cells constitute nearly half of the mammalian nervous system's cellular composition. The glia in C. elegans perform majority of tasks comparable to those conducted by their mammalian equivalents. The cephalic sheath (CEPsh) glia, which are known to be the counterparts of mammalian astrocytes, are enriched with two nuclear hormone receptors (NHRs)-NHR-210 and NHR-231. This unique enrichment makes the CEPsh glia and these NHRs intriguing subjects of study concerning neuronal health. We endeavored to assess the role of these NHRs in neurodegenerative diseases and related functional processes, using transgenic C. elegans expressing human alpha-synuclein. We employed RNAi-mediated silencing, followed by behavioural, functional, and metabolic profiling in relation to suppression of NHR-210 and 231. Our findings revealed that depleting nhr-210 changes dopamine-associated behaviour and mitochondrial function in human alpha synuclein-expressing strains NL5901 and UA44, through a putative target, pgp-9, a transmembrane transporter. Considering the alteration in mitochondrial function and the involvement of a transmembrane transporter, we performed metabolomics study via HR-MAS NMR spectroscopy. Remarkably, substantial modifications in ATP, betaine, lactate, and glycine levels were seen upon the absence of nhr-210. We also detected considerable changes in metabolic pathways such as phenylalanine, tyrosine, and tryptophan biosynthesis metabolism; glycine, serine, and threonine metabolism; as well as glyoxalate and dicarboxylate metabolism. In conclusion, the deficiency of the nuclear hormone receptor nhr-210 in alpha-synuclein expressing strain of C. elegans, results in altered mitochondrial function, coupled with alterations in vital metabolite levels. These findings underline the functional and physiological importance of nhr-210 enrichment in CEPsh glia.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38691171/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38691171</a> | DOI:<a href=https://doi.org/10.1007/s00018-024-05179-2>10.1007/s00018-024-05179-2</a></p></div>]]></content:encoded>
  19.      <guid isPermaLink="false">pubmed:38691171</guid>
  20.      <pubDate>Wed, 01 May 2024 06:00:00 -0400</pubDate>
  21.      <dc:creator>Rohil Hameed</dc:creator>
  22.      <dc:creator>Anam Naseer</dc:creator>
  23.      <dc:creator>Ankit Saxena</dc:creator>
  24.      <dc:creator>Mahmood Akbar</dc:creator>
  25.      <dc:creator>Pranoy Toppo</dc:creator>
  26.      <dc:creator>Arunabh Sarkar</dc:creator>
  27.      <dc:creator>Sanjeev K Shukla</dc:creator>
  28.      <dc:creator>Aamir Nazir</dc:creator>
  29.      <dc:date>2024-05-01</dc:date>
  30.      <dc:source>Cellular and molecular life sciences : CMLS</dc:source>
  31.      <dc:title>Functional implications of NHR-210 enrichment in C. elegans cephalic sheath glia: insights into metabolic and mitochondrial disruptions in Parkinson's disease models</dc:title>
  32.      <dc:identifier>pmid:38691171</dc:identifier>
  33.      <dc:identifier>doi:10.1007/s00018-024-05179-2</dc:identifier>
  34.    </item>
  35.    <item>
  36.      <title>Faster, More Practical, but Still Accurate: Deep Learning for Diagnosis of Progressive Supranuclear Palsy</title>
  37.      <link>https://pubmed.ncbi.nlm.nih.gov/38691010/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  38.      <description>No abstract</description>
  39.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Radiol Artif Intell. 2024 May;6(3):e240181. doi: 10.1148/ryai.240181.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38691010/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38691010</a> | DOI:<a href=https://doi.org/10.1148/ryai.240181>10.1148/ryai.240181</a></p></div>]]></content:encoded>
  40.      <guid isPermaLink="false">pubmed:38691010</guid>
  41.      <pubDate>Wed, 01 May 2024 06:00:00 -0400</pubDate>
  42.      <dc:creator>Bahram Mohajer</dc:creator>
  43.      <dc:date>2024-05-01</dc:date>
  44.      <dc:source>Radiology. Artificial intelligence</dc:source>
  45.      <dc:title>Faster, More Practical, but Still Accurate: Deep Learning for Diagnosis of Progressive Supranuclear Palsy</dc:title>
  46.      <dc:identifier>pmid:38691010</dc:identifier>
  47.      <dc:identifier>doi:10.1148/ryai.240181</dc:identifier>
  48.    </item>
  49.    <item>
  50.      <title>Eye movements as predictor of cognitive improvement after cognitive remediation therapy in patients with schizophrenia</title>
  51.      <link>https://pubmed.ncbi.nlm.nih.gov/38690204/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  52.      <description>CONCLUSION: Eye movements as a non-invasiveness, objective, and sensitive method of evaluating cognitive function, and combined saccadic measurements in pro- and anti-saccades tasks could be more beneficial than free-viewing task in predicting the effect of CRT on cognitive improvement in patients with schizophrenia.</description>
  53.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Front Psychiatry. 2024 Apr 16;15:1395198. doi: 10.3389/fpsyt.2024.1395198. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">AIM: Baseline cognitive functions of patients predicted the efficacy of cognitive remediation therapy (CRT), but results are mixed. Eye movement is a more objective and advanced assessment of cognitive functions than neuropsychological testing. We aimed to investigate the applicability of eye movements in predicting cognitive improvement after patients with schizophrenia were treated with CRT.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We recruited 79 patients with schizophrenia to complete 8 weeks of CRT and assessed their cognitive improvement outcomes. Eye movements were assessed by prosaccades, antisaccades, and free-viewing tasks at baseline, and neuropsychological tests in four cognitive domains were assessed before and after treatment to calculate treatment outcomes. Predictors of demographic information, clinical characteristics, and eye movement measures at baseline on cognitive improvement outcomes were analyzed using logistic regression analysis. We further compared the predictive performance between eye movement measurements and neuropsychological test regarding the effect of CRT on cognitive improvement, and explored factors that could be affect the treatment outcomes in different cognitive domains.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: As operationally defined, 33 patients showed improved in cognition (improved group) and 46 patients did not (non-improved group) after CRT. Patients with schizophrenia being employed, lower directional error rate in antisaccade task, and lower the gap effect (i.e., the difference in saccadic latency between the gap condition and overlap condition) in prosaccade task at baseline predicted cognitive improvement in CRT. However, performance in the free-viewing task not associated with cognitive improvement in patients in CRT. Our results show that eye-movement prediction model predicted the effect of CRT on cognitive improvement in patients with schizophrenia better than neuropsychological prediction model in CRT. In addition, baseline eye-movements, cognitive reserve, antipsychotic medication dose, anticholinergic cognitive burden change, and number of training sessions were associated with improvements in four cognitive domains.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Eye movements as a non-invasiveness, objective, and sensitive method of evaluating cognitive function, and combined saccadic measurements in pro- and anti-saccades tasks could be more beneficial than free-viewing task in predicting the effect of CRT on cognitive improvement in patients with schizophrenia.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38690204/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38690204</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11059054/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11059054</a> | DOI:<a href=https://doi.org/10.3389/fpsyt.2024.1395198>10.3389/fpsyt.2024.1395198</a></p></div>]]></content:encoded>
  54.      <guid isPermaLink="false">pubmed:38690204</guid>
  55.      <pubDate>Wed, 01 May 2024 06:00:00 -0400</pubDate>
  56.      <dc:creator>Jiahui Zhu</dc:creator>
  57.      <dc:creator>Jinhao Li</dc:creator>
  58.      <dc:creator>Li Zhou</dc:creator>
  59.      <dc:creator>Lingzi Xu</dc:creator>
  60.      <dc:creator>Chengcheng Pu</dc:creator>
  61.      <dc:creator>Bingjie Huang</dc:creator>
  62.      <dc:creator>Qi Zhou</dc:creator>
  63.      <dc:creator>Yunhan Lin</dc:creator>
  64.      <dc:creator>Yajing Tang</dc:creator>
  65.      <dc:creator>Liu Yang</dc:creator>
  66.      <dc:creator>Chuan Shi</dc:creator>
  67.      <dc:date>2024-05-01</dc:date>
  68.      <dc:source>Frontiers in psychiatry</dc:source>
  69.      <dc:title>Eye movements as predictor of cognitive improvement after cognitive remediation therapy in patients with schizophrenia</dc:title>
  70.      <dc:identifier>pmid:38690204</dc:identifier>
  71.      <dc:identifier>pmc:PMC11059054</dc:identifier>
  72.      <dc:identifier>doi:10.3389/fpsyt.2024.1395198</dc:identifier>
  73.    </item>
  74.    <item>
  75.      <title>Parkinson's disease - The dentist's role as part of the healthcare team</title>
  76.      <link>https://pubmed.ncbi.nlm.nih.gov/38689457/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  77.      <description>Parkinson's disease is a neurodegenerative disease that results in patients exhibiting uncontrolled movements, changes in saliva production, and difficulty in swallowing and speech. Understanding the staging of the disease and the available therapies allows dentists to treat these patients safely and with compassion to meet their oral health care needs for an optimal quality of life. This appraisal discusses Parkinson's disease as it relates to clinically relevant facts to manage and treat the...</description>
  78.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Prosthodont. 2024 Apr 30. doi: 10.1111/jopr.13862. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Parkinson's disease is a neurodegenerative disease that results in patients exhibiting uncontrolled movements, changes in saliva production, and difficulty in swallowing and speech. Understanding the staging of the disease and the available therapies allows dentists to treat these patients safely and with compassion to meet their oral health care needs for an optimal quality of life. This appraisal discusses Parkinson's disease as it relates to clinically relevant facts to manage and treat the oral health care needs of these patients in the short and long term including general dental care recommendations. Important observations related to Parkinson's disease include disease causation,; stages, pharmacologic treatment, the effects on saliva, mastication, dysphagia, and aspiration pneumonia. Dental recommendations are made for the dentate, the partially edentulous, and the completely edentulous Parkinson's patients with a focus on late-stage concerns. Optimizing dental health will help maintain the quality of life as the disease progresses. In late stages of Parkinson's disease, dental treatment should focus on keeping the patient comfortable and out of pain. While benign neglect is an often-used term, compassionate therapy in the late stages of Parkinson's disease is a more compelling term for defining the patient's needs. Since dysphagia in Parkinson's patients has been underdiagnosed, neurologists must be aware of the important part that dentists play in the early diagnosis for these patients. Early referral to a dentist is vital to mitigate the unfortunate consequence of the need for extensive dental care in late-stage patients.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689457/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689457</a> | DOI:<a href=https://doi.org/10.1111/jopr.13862>10.1111/jopr.13862</a></p></div>]]></content:encoded>
  79.      <guid isPermaLink="false">pubmed:38689457</guid>
  80.      <pubDate>Wed, 01 May 2024 06:00:00 -0400</pubDate>
  81.      <dc:creator>Liliana Ortiz Camacho</dc:creator>
  82.      <dc:creator>Leila Jahangiri</dc:creator>
  83.      <dc:creator>Jenna Iseringhausen</dc:creator>
  84.      <dc:creator>Gary R Goldstein</dc:creator>
  85.      <dc:date>2024-05-01</dc:date>
  86.      <dc:source>Journal of prosthodontics : official journal of the American College of Prosthodontists</dc:source>
  87.      <dc:title>Parkinson's disease - The dentist's role as part of the healthcare team</dc:title>
  88.      <dc:identifier>pmid:38689457</dc:identifier>
  89.      <dc:identifier>doi:10.1111/jopr.13862</dc:identifier>
  90.    </item>
  91.    <item>
  92.      <title>The impact of anxiety on gait impairments in Parkinson's disease: insights from sensor-based gait analysis</title>
  93.      <link>https://pubmed.ncbi.nlm.nih.gov/38689288/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  94.      <description>CONCLUSION: Our study discovered that anxiety has a significant impact on gait impairments in PD patients, especially exacerbating shuffling steps and prolonging stance phase. These findings highlight the importance of addressing anxiety in PD precision therapy to achieve better treatment outcomes.</description>
  95.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Neuroeng Rehabil. 2024 Apr 30;21(1):68. doi: 10.1186/s12984-024-01364-3.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Sensor-based gait analysis provides a robust quantitative tool for assessing gait impairments and their associated factors in Parkinson's disease (PD). Anxiety is observed to interfere with gait clinically, but this has been poorly investigated. Our purpose is to utilize gait analysis to uncover the effect of anxiety on gait in patients with PD.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We enrolled 38 and 106 PD patients with and without anxiety, respectively. Gait parameters were quantitively examined and compared between two groups both in single-task (ST) and dual-task (DT) walking tests. Multiple linear regression was applied to evaluate whether anxiety independently contributed to gait impairments.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: During ST, PD patients with anxiety presented significantly shorter stride length, lower gait velocity, longer stride time and stance time, longer stance phase, smaller toe-off (TO) and heel-strike (HS) angles than those without anxiety. While under DT status, the differences were diminished. Multiple linear regression analysis demonstrated that anxiety was an independent factor to a serials of gait parameters, particularly ST-TO (B = -2.599, (-4.82, -0.38)), ST-HS (B = -2.532, (-4.71, -0.35)), ST-TO-CV (B = 4.627, (1.71, 7.64)), ST-HS-CV(B = 4.597, (1.66, 7.53)), ST stance phase (B = 1.4, (0.22, 2.58)), and DT stance phase (B = 1.749, (0.56, 2.94)).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: Our study discovered that anxiety has a significant impact on gait impairments in PD patients, especially exacerbating shuffling steps and prolonging stance phase. These findings highlight the importance of addressing anxiety in PD precision therapy to achieve better treatment outcomes.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689288/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689288</a> | DOI:<a href=https://doi.org/10.1186/s12984-024-01364-3>10.1186/s12984-024-01364-3</a></p></div>]]></content:encoded>
  96.      <guid isPermaLink="false">pubmed:38689288</guid>
  97.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  98.      <dc:creator>Xiaodan Zhang</dc:creator>
  99.      <dc:creator>Yulan Jin</dc:creator>
  100.      <dc:creator>Mateng Wang</dc:creator>
  101.      <dc:creator>Chengcheng Ji</dc:creator>
  102.      <dc:creator>Zhaoying Chen</dc:creator>
  103.      <dc:creator>Weinv Fan</dc:creator>
  104.      <dc:creator>Timothy Hudson Rainer</dc:creator>
  105.      <dc:creator>Qiongfeng Guan</dc:creator>
  106.      <dc:creator>Qianyun Li</dc:creator>
  107.      <dc:date>2024-04-30</dc:date>
  108.      <dc:source>Journal of neuroengineering and rehabilitation</dc:source>
  109.      <dc:title>The impact of anxiety on gait impairments in Parkinson's disease: insights from sensor-based gait analysis</dc:title>
  110.      <dc:identifier>pmid:38689288</dc:identifier>
  111.      <dc:identifier>doi:10.1186/s12984-024-01364-3</dc:identifier>
  112.    </item>
  113.    <item>
  114.      <title>Medication adherence and costs of medical care among patients with Parkinson's disease: an observational study using electronic medical records</title>
  115.      <link>https://pubmed.ncbi.nlm.nih.gov/38689223/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  116.      <description>CONCLUSIONS: APD adherence rate among Chinese patients with PD was moderate and related primarily to age, comorbidities, and healthcare costs. The factors should be considered when prescribing APDs.</description>
  117.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Public Health. 2024 Apr 30;24(1):1202. doi: 10.1186/s12889-024-18431-y.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Adherence to antiparkinsonian drugs (APDs) is critical for patients with Parkinson's disease (PD), for which medication is the main therapeutic strategy. Previous studies have focused on specific disorders in a single system when assessing clinical factors affecting adherence to PD treatment, and no international comparative data are available on the medical costs for Chinese patients with PD. The present study aimed to evaluate medication adherence and its associated factors among Chinese patients with PD using a systematic approach and to explore the impact of adequate medication adherence on direct medical costs.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: A retrospective analysis was conducted using the electronic medical records of patients with PD from a medical center in China. Patients with a minimum of two APD prescriptions from January 1, 2016 to August 15, 2018 were included. Medication possession ratio (MPR) and proportion of days covered were used to measure APD adherence. Multiple linear regression analysis was used to identify factors affecting APD adherence. Gamma regression analysis was used to explore the impact of APD adherence on direct medical costs.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: In total, 1,712 patients were included in the study, and the mean MPR was 0.68 (± 0.25). Increased number of APDs and all medications, and higher daily levodopa-equivalent doses resulted in higher MPR (mean difference [MD] = 0.04 [0.03-0.05]; MD = 0.02 [0.01-0.03]; MD = 0.03 [0.01-0.04], respectively); combined digestive system diseases, epilepsy, or older age resulted in lower MPR (MD = -0.06 [-0.09 to -0.03]; MD = -0.07 [-0.14 to -0.01]; MD = -0.02 [-0.03 to -0.01], respectively). Higher APD adherence resulted in higher direct medical costs, including APD and other outpatient costs. For a 0.3 increase in MPR, the two costs increased by $34.42 ($25.43-$43.41) and $14.63 ($4.86-$24.39) per year, respectively.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: APD adherence rate among Chinese patients with PD was moderate and related primarily to age, comorbidities, and healthcare costs. The factors should be considered when prescribing APDs.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689223/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689223</a> | DOI:<a href=https://doi.org/10.1186/s12889-024-18431-y>10.1186/s12889-024-18431-y</a></p></div>]]></content:encoded>
  118.      <guid isPermaLink="false">pubmed:38689223</guid>
  119.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  120.      <dc:creator>Zhanmiao Yi</dc:creator>
  121.      <dc:creator>Yudan Mao</dc:creator>
  122.      <dc:creator>Chenxuan He</dc:creator>
  123.      <dc:creator>Yantao Zhang</dc:creator>
  124.      <dc:creator>Junwen Zhou</dc:creator>
  125.      <dc:creator>Xing Lin Feng</dc:creator>
  126.      <dc:date>2024-04-30</dc:date>
  127.      <dc:source>BMC public health</dc:source>
  128.      <dc:title>Medication adherence and costs of medical care among patients with Parkinson's disease: an observational study using electronic medical records</dc:title>
  129.      <dc:identifier>pmid:38689223</dc:identifier>
  130.      <dc:identifier>doi:10.1186/s12889-024-18431-y</dc:identifier>
  131.    </item>
  132.    <item>
  133.      <title>Variations in the sleep-related breathing disorder index on polysomnography between men with HIV and controls: a matched case-control study</title>
  134.      <link>https://pubmed.ncbi.nlm.nih.gov/38689220/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  135.      <description>CONCLUSIONS: Early detected SRBDs and subtypes in PLWH to begin treatment for the underlying cause could reduce the risk of sleepiness-related traffic accidents.</description>
  136.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Infect Dis. 2024 Apr 30;24(1):456. doi: 10.1186/s12879-024-09322-z.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Both sleep-related breathing disorders (SRBDs) and HIV infection can interfere with normal sleep architecture, and also cause physical and psychological distress. We aimed to understand the differences in the obstructive patterns, sleep architecture, physical and psychological distress when compared between people living with HIV (PLWH) and matched the severity of SRBDs controls.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: A comparative study using matched case-control design was conducted. Men with HIV infection (case group) were enrolled from 2016 to 2019. A control group with HIV seronegative men were matched for SRBDs severity, and were selected from sleep medicine center database for comparison.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The mean age of the 108 men (including 54 cases and 54 matched controls) was 33.75 years. Central-apnea index (CI) was higher in the case group rather than matched controls (mean CI, 0.34 vs. 0.17, p = 0.049). PLWH had a lower mean percentage of stage 3 sleep (10.26% vs. 13.94%, p = 0.034) and a higher percentage of rapid eye movement sleep (20.59% vs. 17.85%, p = 0.011) compared to matched controls. Nocturnal enuresis and sleepiness causing traffic accidents were more frequent complaint in PLWH compared to controls.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Early detected SRBDs and subtypes in PLWH to begin treatment for the underlying cause could reduce the risk of sleepiness-related traffic accidents.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689220/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689220</a> | DOI:<a href=https://doi.org/10.1186/s12879-024-09322-z>10.1186/s12879-024-09322-z</a></p></div>]]></content:encoded>
  137.      <guid isPermaLink="false">pubmed:38689220</guid>
  138.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  139.      <dc:creator>Yen-Chin Chen</dc:creator>
  140.      <dc:creator>Chang-Chun Chen</dc:creator>
  141.      <dc:creator>Wen-Kuei Lin</dc:creator>
  142.      <dc:creator>Han Siong Toh</dc:creator>
  143.      <dc:creator>Nai-Ying Ko</dc:creator>
  144.      <dc:creator>Cheng-Yu Lin</dc:creator>
  145.      <dc:date>2024-04-30</dc:date>
  146.      <dc:source>BMC infectious diseases</dc:source>
  147.      <dc:title>Variations in the sleep-related breathing disorder index on polysomnography between men with HIV and controls: a matched case-control study</dc:title>
  148.      <dc:identifier>pmid:38689220</dc:identifier>
  149.      <dc:identifier>doi:10.1186/s12879-024-09322-z</dc:identifier>
  150.    </item>
  151.    <item>
  152.      <title>Multidisciplinary analysis of cancer-related fatigue at the time of diagnosis: preliminary results of the BIOCARE FActory cohort</title>
  153.      <link>https://pubmed.ncbi.nlm.nih.gov/38689167/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  154.      <description>CONCLUSION: At the time of diagnosis, emotional and cognitive dimensions are over-represented compared to the general population, and specific subdimensions have specific predictors that support the idea of distinct mechanisms. Evaluating CRF subdimensions and their potential mechanisms at the time of diagnosis would be particularly relevant for identifying high-risk patients and offering them appropriate interventions.</description>
  155.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Support Care Cancer. 2024 Apr 30;32(5):319. doi: 10.1007/s00520-024-08520-4.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">PURPOSE: Cancer-related fatigue (CRF) is a common side effect of cancer and cancer treatment that significantly impairs the quality of life and can persist for years after treatment completion. Although fatigue is often associated with cancer treatment, it is also a result of the disease itself, even before intervention. CRF at the time of diagnosis may affect treatment timing or completion and is a consistent predictor of post-treatment fatigue at any time. The mechanisms underlying CRF are multidimensional and not well understood, particularly at the time of diagnosis.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Sixty-five breast cancer patients at the time of diagnosis were included. The participants completed self-assessment questionnaires about CRF, sleep disturbances, and emotional symptoms and wore an accelerometer to assess levels of spontaneous physical activity and sleep quality. During the experimental session, the participants underwent cognitive, neuromuscular, and exercise metabolism evaluations.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Using augmented backward elimination regression, this study found that emotional symptoms and perceived sleep disturbances were the strongest predictors of CRF (adjusted r<sup>2</sup> = 0.51). Neuromuscular fatigability and sleep disturbance were also associated with physical dimensions, whereas cognitive performance was associated with cognitive dimensions.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: At the time of diagnosis, emotional and cognitive dimensions are over-represented compared to the general population, and specific subdimensions have specific predictors that support the idea of distinct mechanisms. Evaluating CRF subdimensions and their potential mechanisms at the time of diagnosis would be particularly relevant for identifying high-risk patients and offering them appropriate interventions.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">TRIAL REGISTRATION: This study was registered at ClinicalTrials.gov (NCT04391543) in May, 2020.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689167/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689167</a> | DOI:<a href=https://doi.org/10.1007/s00520-024-08520-4>10.1007/s00520-024-08520-4</a></p></div>]]></content:encoded>
  156.      <guid isPermaLink="false">pubmed:38689167</guid>
  157.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  158.      <dc:creator>A Leclercq</dc:creator>
  159.      <dc:creator>A Chatrenet</dc:creator>
  160.      <dc:creator>H Bourgeois</dc:creator>
  161.      <dc:creator>O Cojocarasu</dc:creator>
  162.      <dc:creator>C Mathie</dc:creator>
  163.      <dc:creator>T Martin</dc:creator>
  164.      <dc:creator>A Rahmani</dc:creator>
  165.      <dc:creator>B Morel</dc:creator>
  166.      <dc:date>2024-04-30</dc:date>
  167.      <dc:source>Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer</dc:source>
  168.      <dc:title>Multidisciplinary analysis of cancer-related fatigue at the time of diagnosis: preliminary results of the BIOCARE FActory cohort</dc:title>
  169.      <dc:identifier>pmid:38689167</dc:identifier>
  170.      <dc:identifier>doi:10.1007/s00520-024-08520-4</dc:identifier>
  171.    </item>
  172.    <item>
  173.      <title>Longitudinal study investigating the influence of COMT gene polymorphism on cortical thickness changes in Parkinson's disease over four years</title>
  174.      <link>https://pubmed.ncbi.nlm.nih.gov/38689006/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  175.      <description>Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting over 3% of those over 65. It's caused by reduced dopaminergic neurons and Lewy bodies, leading to motor and non-motor symptoms. The relationship between COMT gene polymorphisms and PD is complex and not fully elucidated. Some studies have reported associations between certain COMT gene variants and PD risk, while others have not found significant associations. This study investigates how COMT gene variations impact...</description>
  176.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 Apr 30;14(1):9920. doi: 10.1038/s41598-024-60828-7.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Parkinson's disease (PD) is a progressive neurodegenerative disorder affecting over 3% of those over 65. It's caused by reduced dopaminergic neurons and Lewy bodies, leading to motor and non-motor symptoms. The relationship between COMT gene polymorphisms and PD is complex and not fully elucidated. Some studies have reported associations between certain COMT gene variants and PD risk, while others have not found significant associations. This study investigates how COMT gene variations impact cortical thickness changes in PD patients over time, aiming to link genetic factors, especially COMT gene variations, with PD progression. This study analyzed data from 44 PD patients with complete 4-year imaging follow-up from the Parkinson Progression Marker Initiative (PPMI) database. Magnetic resonance imaging (MRI) scans were acquired using consistent methods across 9 different MRI scanners. COMT single-nucleotide polymorphisms (SNPs) were assessed based on whole genome sequencing data. Longitudinal image analysis was conducted using FreeSurfer's processing pipeline. Linear mixed-effect models were employed to examine the interaction effect of genetic variations and time on cortical thickness, while controlling for covariates and subject-specific variations. The rs165599 SNP stands out as a potential contributor to alterations in cortical thickness, showing a significant reduction in overall mean cortical thickness in both hemispheres in homozygotes (Left: P = 0.023, Right: P = 0.028). The supramarginal, precentral, and superior frontal regions demonstrated significant bilateral alterations linked to rs165599. Our findings suggest that the rs165599 variant leads to earlier manifestation of cortical thinning during the course of the disease. However, it does not result in more severe cortical thinning outcomes over time. There is a need for larger cohorts and control groups to validate these findings and consider genetic variant interactions and clinical features to elucidate the specific mechanisms underlying COMT-related neurodegenerative processes in PD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38689006/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38689006</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60828-7>10.1038/s41598-024-60828-7</a></p></div>]]></content:encoded>
  177.      <guid isPermaLink="false">pubmed:38689006</guid>
  178.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  179.      <dc:creator>Amin Tajerian</dc:creator>
  180.      <dc:date>2024-04-30</dc:date>
  181.      <dc:source>Scientific reports</dc:source>
  182.      <dc:title>Longitudinal study investigating the influence of COMT gene polymorphism on cortical thickness changes in Parkinson's disease over four years</dc:title>
  183.      <dc:identifier>pmid:38689006</dc:identifier>
  184.      <dc:identifier>doi:10.1038/s41598-024-60828-7</dc:identifier>
  185.    </item>
  186.    <item>
  187.      <title>Protein mimetic 2D FAST rescues alpha synuclein aggregation mediated early and post disease Parkinson's phenotypes</title>
  188.      <link>https://pubmed.ncbi.nlm.nih.gov/38688913/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  189.      <description>Abberent protein-protein interactions potentiate many diseases and one example is the toxic, self-assembly of α-Synuclein in the dopaminergic neurons of patients with Parkinson's disease; therefore, a potential therapeutic strategy is the small molecule modulation of α-Synuclein aggregation. In this work, we develop an Oligopyridylamide based 2-dimensional Fragment-Assisted Structure-based Technique to identify antagonists of α-Synuclein aggregation. The technique utilizes a fragment-based...</description>
  190.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Nat Commun. 2024 Apr 30;15(1):3658. doi: 10.1038/s41467-024-47980-4.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Abberent protein-protein interactions potentiate many diseases and one example is the toxic, self-assembly of α-Synuclein in the dopaminergic neurons of patients with Parkinson's disease; therefore, a potential therapeutic strategy is the small molecule modulation of α-Synuclein aggregation. In this work, we develop an Oligopyridylamide based 2-dimensional Fragment-Assisted Structure-based Technique to identify antagonists of α-Synuclein aggregation. The technique utilizes a fragment-based screening of an extensive array of non-proteinogenic side chains in Oligopyridylamides, leading to the identification of NS132 as an antagonist of the multiple facets of α-Synuclein aggregation. We further identify a more cell permeable analog (NS163) without sacrificing activity. Oligopyridylamides rescue α-Synuclein aggregation mediated Parkinson's disease phenotypes in dopaminergic neurons in early and post disease Caenorhabditis elegans models. We forsee tremendous potential in our technique to identify lead therapeutics for Parkinson's disease and other diseases as it is expandable to other oligoamide scaffolds and a larger array of side chains.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38688913/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38688913</a> | DOI:<a href=https://doi.org/10.1038/s41467-024-47980-4>10.1038/s41467-024-47980-4</a></p></div>]]></content:encoded>
  191.      <guid isPermaLink="false">pubmed:38688913</guid>
  192.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  193.      <dc:creator>Nicholas H Stillman</dc:creator>
  194.      <dc:creator>Johnson A Joseph</dc:creator>
  195.      <dc:creator>Jemil Ahmed</dc:creator>
  196.      <dc:creator>Charles Zuwu Baysah</dc:creator>
  197.      <dc:creator>Ryan A Dohoney</dc:creator>
  198.      <dc:creator>Tyler D Ball</dc:creator>
  199.      <dc:creator>Alexandra G Thomas</dc:creator>
  200.      <dc:creator>Tessa C Fitch</dc:creator>
  201.      <dc:creator>Courtney M Donnelly</dc:creator>
  202.      <dc:creator>Sunil Kumar</dc:creator>
  203.      <dc:date>2024-04-30</dc:date>
  204.      <dc:source>Nature communications</dc:source>
  205.      <dc:title>Protein mimetic 2D FAST rescues alpha synuclein aggregation mediated early and post disease Parkinson's phenotypes</dc:title>
  206.      <dc:identifier>pmid:38688913</dc:identifier>
  207.      <dc:identifier>doi:10.1038/s41467-024-47980-4</dc:identifier>
  208.    </item>
  209.    <item>
  210.      <title>Adult-onset acute rheumatic fever with chorea and carditis</title>
  211.      <link>https://pubmed.ncbi.nlm.nih.gov/38688571/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  212.      <description>Rheumatic fever is a major cause of cardiovascular morbidity and mortality in low-income and middle-income countries, and it usually occurs at a young age. Adult-onset acute rheumatic fever is a rare condition and usually represents a recurrence of childhood-onset disease. We report a case of an elderly man presenting with rheumatic carditis and rheumatic chorea subsequently diagnosed with adult-onset rheumatic fever.</description>
  213.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMJ Case Rep. 2024 Apr 30;17(4):e258920. doi: 10.1136/bcr-2023-258920.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Rheumatic fever is a major cause of cardiovascular morbidity and mortality in low-income and middle-income countries, and it usually occurs at a young age. Adult-onset acute rheumatic fever is a rare condition and usually represents a recurrence of childhood-onset disease. We report a case of an elderly man presenting with rheumatic carditis and rheumatic chorea subsequently diagnosed with adult-onset rheumatic fever.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38688571/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38688571</a> | DOI:<a href=https://doi.org/10.1136/bcr-2023-258920>10.1136/bcr-2023-258920</a></p></div>]]></content:encoded>
  214.      <guid isPermaLink="false">pubmed:38688571</guid>
  215.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  216.      <dc:creator>Hasara Jayasekara</dc:creator>
  217.      <dc:creator>Janitha Sampath Wickramarathne</dc:creator>
  218.      <dc:creator>Peduru Arachchige Jayasinghe</dc:creator>
  219.      <dc:date>2024-04-30</dc:date>
  220.      <dc:source>BMJ case reports</dc:source>
  221.      <dc:title>Adult-onset acute rheumatic fever with chorea and carditis</dc:title>
  222.      <dc:identifier>pmid:38688571</dc:identifier>
  223.      <dc:identifier>doi:10.1136/bcr-2023-258920</dc:identifier>
  224.    </item>
  225.    <item>
  226.      <title>Neurosurgical neuromodulation therapy for psychiatric disorders</title>
  227.      <link>https://pubmed.ncbi.nlm.nih.gov/38688105/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  228.      <description>Psychiatric disorders are among the leading contributors to global disease burden and disability. A significant portion of patients with psychiatric disorders remain treatment-refractory to best available therapy. With insights from the neurocircuitry of psychiatric disorders and extensive experience of neuromodulation with deep brain stimulation (DBS) in movement disorders, DBS is increasingly being considered to modulate the neural network in psychiatric disorders. Currently,...</description>
  229.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurotherapeutics. 2024 Apr 29;21(3):e00366. doi: 10.1016/j.neurot.2024.e00366. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Psychiatric disorders are among the leading contributors to global disease burden and disability. A significant portion of patients with psychiatric disorders remain treatment-refractory to best available therapy. With insights from the neurocircuitry of psychiatric disorders and extensive experience of neuromodulation with deep brain stimulation (DBS) in movement disorders, DBS is increasingly being considered to modulate the neural network in psychiatric disorders. Currently, obsessive-compulsive disorder (OCD) is the only U.S. FDA (United States Food and Drug Administration) approved DBS indication for psychiatric disorders. Medically refractory depression, addiction, and other psychiatric disorders are being explored for DBS neuromodulation. Studies evaluating DBS for psychiatric disorders are promising but lack larger, controlled studies. This paper presents a brief review and the current state of DBS and other neurosurgical neuromodulation therapies for OCD and other psychiatric disorders. We also present a brief review of MR-guided Focused Ultrasound (MRgFUS), a novel form of neurosurgical neuromodulation, which can target deep subcortical structures similar to DBS, but in a noninvasive fashion. Early experiences of neurosurgical neuromodulation therapies, including MRgFUS neuromodulation are encouraging in psychiatric disorders; however, they remain investigational. Currently, DBS and VNS are the only FDA approved neurosurgical neuromodulation options in properly selected cases of OCD and depression, respectively.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38688105/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38688105</a> | DOI:<a href=https://doi.org/10.1016/j.neurot.2024.e00366>10.1016/j.neurot.2024.e00366</a></p></div>]]></content:encoded>
  230.      <guid isPermaLink="false">pubmed:38688105</guid>
  231.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  232.      <dc:creator>Manish Ranjan</dc:creator>
  233.      <dc:creator>James J Mahoney</dc:creator>
  234.      <dc:creator>Ali R Rezai</dc:creator>
  235.      <dc:date>2024-04-30</dc:date>
  236.      <dc:source>Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics</dc:source>
  237.      <dc:title>Neurosurgical neuromodulation therapy for psychiatric disorders</dc:title>
  238.      <dc:identifier>pmid:38688105</dc:identifier>
  239.      <dc:identifier>doi:10.1016/j.neurot.2024.e00366</dc:identifier>
  240.    </item>
  241.    <item>
  242.      <title>Ictal Direct Current Shifts Preceded Much Earlier Than High Frequency Oscillations After Status: Is It the Effect of Status or Antiseizure Medication?</title>
  243.      <link>https://pubmed.ncbi.nlm.nih.gov/38687304/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  244.      <description>CONCLUSIONS: The attenuation of ictal DC shifts and HFOs after ASM loading implies that astrocyte and neuronal activity may be both attenuated by ASMs. This finding may help with our understanding of the pathophysiology of epilepsy and can aid with the discovery of new approaches for epilepsy management.</description>
  245.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Clin Neurophysiol. 2024 Apr 26. doi: 10.1097/WNP.0000000000001087. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">PURPOSE: While spikes and sharp waves are considered as markers of epilepsy in conventional electroencephalography, ictal direct current (DC) shifts and high-frequency oscillations (HFOs) appear to be useful biomarkers for epileptogenicity. We analyzed how ictal DC shifts and HFOs were affected by focal status epilepticus and antiseizure medications (ASMs).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: A 20-year-old female patient who underwent long-term intracranial electrode implantation for epilepsy surgery presented with 72 habitual seizures and a focal status epilepticus episode lasting for 4 h. Ten, 3, and 10 consecutive habitual seizures were analyzed before the status, after the status, and after ASM (valproate) loading, respectively.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Before and immediately after the status, ictal DC shifts remained the same in terms of the amplitude, duration, and slope of DC shifts. High-frequency oscillations also remained the same in terms of the duration, frequency, and power except for the power of the lower frequency band. After ASM loading, the duration, amplitude, and slope of the ictal DC shift were significantly attenuated. The duration, frequency, and power of the HFOs were significantly attenuated. Furthermore, the interval between the DC onset and HFO onset was significantly longer and the interval between the HFO onset and ictal DC shift peak was significantly shorter.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: The attenuation of ictal DC shifts and HFOs after ASM loading implies that astrocyte and neuronal activity may be both attenuated by ASMs. This finding may help with our understanding of the pathophysiology of epilepsy and can aid with the discovery of new approaches for epilepsy management.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38687304/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38687304</a> | DOI:<a href=https://doi.org/10.1097/WNP.0000000000001087>10.1097/WNP.0000000000001087</a></p></div>]]></content:encoded>
  246.      <guid isPermaLink="false">pubmed:38687304</guid>
  247.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  248.      <dc:creator>Kyoko Kanazawa</dc:creator>
  249.      <dc:creator>Shunsuke Kajikawa</dc:creator>
  250.      <dc:creator>Riki Matsumoto</dc:creator>
  251.      <dc:creator>Miwa Takatani</dc:creator>
  252.      <dc:creator>Mitsuyoshi Nakatani</dc:creator>
  253.      <dc:creator>Masako Daifu-Kobayashi</dc:creator>
  254.      <dc:creator>Hisaji Imamura</dc:creator>
  255.      <dc:creator>Takeharu Kunieda</dc:creator>
  256.      <dc:creator>Susumu Miyamoto</dc:creator>
  257.      <dc:creator>Ryosuke Takahashi</dc:creator>
  258.      <dc:creator>Masao Matsuhashi</dc:creator>
  259.      <dc:creator>Akio Ikeda</dc:creator>
  260.      <dc:date>2024-04-30</dc:date>
  261.      <dc:source>Journal of clinical neurophysiology : official publication of the American Electroencephalographic Society</dc:source>
  262.      <dc:title>Ictal Direct Current Shifts Preceded Much Earlier Than High Frequency Oscillations After Status: Is It the Effect of Status or Antiseizure Medication?</dc:title>
  263.      <dc:identifier>pmid:38687304</dc:identifier>
  264.      <dc:identifier>doi:10.1097/WNP.0000000000001087</dc:identifier>
  265.    </item>
  266.    <item>
  267.      <title>Medical Infomercials</title>
  268.      <link>https://pubmed.ncbi.nlm.nih.gov/38687272/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  269.      <description>No abstract</description>
  270.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">R I Med J (2013). 2024 May 2;107(5):62-63.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38687272/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38687272</a></p></div>]]></content:encoded>
  271.      <guid isPermaLink="false">pubmed:38687272</guid>
  272.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  273.      <dc:creator>Joseph H Friedman</dc:creator>
  274.      <dc:date>2024-04-30</dc:date>
  275.      <dc:source>Rhode Island medical journal (2013)</dc:source>
  276.      <dc:title>Medical Infomercials</dc:title>
  277.      <dc:identifier>pmid:38687272</dc:identifier>
  278.    </item>
  279.    <item>
  280.      <title>Genetic Determined Iron Starvation Signature in Friedreich's Ataxia</title>
  281.      <link>https://pubmed.ncbi.nlm.nih.gov/38686449/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  282.      <description>CONCLUSIONS: We provide evidence for a previously unrecognized iron starvation signature at systemic and cellular levels in FA patients, which is related to the underlying genetic severity. These findings challenge the use of systemic iron lowering therapies in FA. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.</description>
  283.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mov Disord. 2024 Apr 30. doi: 10.1002/mds.29819. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Early studies in cellular models suggested an iron accumulation in Friedreich's ataxia (FA), yet findings from patients are lacking.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: The objective is to characterize systemic iron metabolism, body iron storages, and intracellular iron regulation in FA patients.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: In FA patients and matched healthy controls, we assessed serum iron parameters, regulatory hormones as well as the expression of regulatory proteins and iron distribution in peripheral blood mononuclear cells (PBMCs). We applied magnetic resonance imaging with R<sub>2</sub>*-relaxometry to quantify iron storages in the liver, spleen, and pancreas. Across all evaluations, we assessed the influence of the genetic severity as expressed by the length of the shorter GAA-expansion (GAA1).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: We recruited 40 FA patients (19 women). Compared to controls, FA patients displayed lower serum iron and transferrin saturation. Serum ferritin, hepcidin, mean corpuscular hemoglobin and mean corpuscular volume in FA inversely correlated with the GAA1-repeat length, indicating iron deficiency and restricted availability for erythropoiesis with increasing genetic severity. R<sub>2</sub>*-relaxometry revealed a reduction of splenic and hepatic iron stores in FA. Liver and spleen R<sub>2</sub>* values inversely correlated with the GAA1-repeat length. FA PBMCs displayed downregulation of ferritin and upregulation of transferrin receptor and divalent metal transporter-1 mRNA, particularly in patients with &gt;500 GAA1-repeats. In FA PBMCs, intracellular iron was not increased, but shifted toward mitochondria.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: We provide evidence for a previously unrecognized iron starvation signature at systemic and cellular levels in FA patients, which is related to the underlying genetic severity. These findings challenge the use of systemic iron lowering therapies in FA. © 2024 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38686449/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38686449</a> | DOI:<a href=https://doi.org/10.1002/mds.29819>10.1002/mds.29819</a></p></div>]]></content:encoded>
  284.      <guid isPermaLink="false">pubmed:38686449</guid>
  285.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  286.      <dc:creator>Manuel Grander</dc:creator>
  287.      <dc:creator>David Haschka</dc:creator>
  288.      <dc:creator>Elisabetta Indelicato</dc:creator>
  289.      <dc:creator>Christian Kremser</dc:creator>
  290.      <dc:creator>Matthias Amprosi</dc:creator>
  291.      <dc:creator>Wolfgang Nachbauer</dc:creator>
  292.      <dc:creator>Benjamin Henninger</dc:creator>
  293.      <dc:creator>Ambra Stefani</dc:creator>
  294.      <dc:creator>Birgit Högl</dc:creator>
  295.      <dc:creator>Christine Fischer</dc:creator>
  296.      <dc:creator>Markus Seifert</dc:creator>
  297.      <dc:creator>Stefan Kiechl</dc:creator>
  298.      <dc:creator>Günter Weiss</dc:creator>
  299.      <dc:creator>Sylvia Boesch</dc:creator>
  300.      <dc:date>2024-04-30</dc:date>
  301.      <dc:source>Movement disorders : official journal of the Movement Disorder Society</dc:source>
  302.      <dc:title>Genetic Determined Iron Starvation Signature in Friedreich's Ataxia</dc:title>
  303.      <dc:identifier>pmid:38686449</dc:identifier>
  304.      <dc:identifier>doi:10.1002/mds.29819</dc:identifier>
  305.    </item>
  306.    <item>
  307.      <title>Effectiveness and Safety of Meridian Activation Remedy System for Alleviating Motor Symptoms in Parkinson's Disease: an Observational Study</title>
  308.      <link>https://pubmed.ncbi.nlm.nih.gov/38686429/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  309.      <description>CONCLUSION: An 8-week MARS intervention improved motor symptoms in PD patients. In particular, improvements in UPDRS Part III scores exhibited large clinically important differences. The findings are encouraging, and a randomized controlled trial will be conducted to determine the efficacy and cost-effectiveness of MARS intervention.</description>
  310.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Acupunct Meridian Stud. 2024 Apr 30;17(2):55-68. doi: 10.51507/j.jams.2024.17.2.55.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Parkinson's disease (PD) lacks disease-modifying drugs or sustainable interventions, creating an unmet treatment need. Investigating complementary and alternative medicines aims to improve PD patients' quality of life by alleviating symptoms and delaying the course of the disease.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: In this single-center, prospective, observational, single-arm study, we aimed to assess the effectiveness and safety of acupuncture combined with exercise therapy and the Meridian Activation Remedy System (MARS).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: From March to October 2021, 13 PD patients with Hoehn and Yahr stages 1 to 3 were recruited. For 8 weeks, MARS intervention was carried out twice a week. T-statistics were used to evaluate functional near-infrared spectroscopy (fNIRS) and GAITRite outcomes. All of the remaining outcome variables were evaluated using the Wilcoxon signed-rank test.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The MARS intervention significantly reduced PD patients' Movement Disorder Society-Sponsored Revision of the Unified Parkinson's Disease Rating Scale (MDSUPDRS) Part III score (from 20.0 ± 11.8 to 8.8 ± 5.5, <i>p</i> = 0.003), 10-meter walk test speed (from 9.5 ± 1.8 to 8.7 ± 1.3 seconds, <i>p</i> = 0.040), and timed up and go time (from 9.8 ± 1.8 to 8.9 ± 1.4 seconds, <i>p</i> = 0.040). Moreover, the MDS-UPDRS Part II, fNIRS hemodynamics, 360-degree turn test, fall efficacy scale, and Parkinson's Disease Questionnaire 39 scores improved but not significantly. All participants completed the 8-week intervention without any adverse reactions.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: An 8-week MARS intervention improved motor symptoms in PD patients. In particular, improvements in UPDRS Part III scores exhibited large clinically important differences. The findings are encouraging, and a randomized controlled trial will be conducted to determine the efficacy and cost-effectiveness of MARS intervention.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38686429/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38686429</a> | DOI:<a href=https://doi.org/10.51507/j.jams.2024.17.2.55>10.51507/j.jams.2024.17.2.55</a></p></div>]]></content:encoded>
  311.      <guid isPermaLink="false">pubmed:38686429</guid>
  312.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  313.      <dc:creator>InWoo Choi</dc:creator>
  314.      <dc:creator>Sangsoo Park</dc:creator>
  315.      <dc:creator>Seung Hyun Lee</dc:creator>
  316.      <dc:creator>Jeong-Woo Seo</dc:creator>
  317.      <dc:creator>In-Chan Seol</dc:creator>
  318.      <dc:creator>Yoon-Sik Kim</dc:creator>
  319.      <dc:creator>Miso S Park</dc:creator>
  320.      <dc:creator>Horyong Yoo</dc:creator>
  321.      <dc:date>2024-04-30</dc:date>
  322.      <dc:source>Journal of acupuncture and meridian studies</dc:source>
  323.      <dc:title>Effectiveness and Safety of Meridian Activation Remedy System for Alleviating Motor Symptoms in Parkinson's Disease: an Observational Study</dc:title>
  324.      <dc:identifier>pmid:38686429</dc:identifier>
  325.      <dc:identifier>doi:10.51507/j.jams.2024.17.2.55</dc:identifier>
  326.    </item>
  327.    <item>
  328.      <title>Exploring Novel Meridian-Based Therapeutic Approaches in Parkinson's Disease</title>
  329.      <link>https://pubmed.ncbi.nlm.nih.gov/38686427/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  330.      <description>No abstract</description>
  331.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Acupunct Meridian Stud. 2024 Apr 30;17(2):45-46. doi: 10.51507/j.jams.2024.17.2.45.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38686427/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38686427</a> | DOI:<a href=https://doi.org/10.51507/j.jams.2024.17.2.45>10.51507/j.jams.2024.17.2.45</a></p></div>]]></content:encoded>
  332.      <guid isPermaLink="false">pubmed:38686427</guid>
  333.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  334.      <dc:creator>Chan-Young Kwon</dc:creator>
  335.      <dc:date>2024-04-30</dc:date>
  336.      <dc:source>Journal of acupuncture and meridian studies</dc:source>
  337.      <dc:title>Exploring Novel Meridian-Based Therapeutic Approaches in Parkinson's Disease</dc:title>
  338.      <dc:identifier>pmid:38686427</dc:identifier>
  339.      <dc:identifier>doi:10.51507/j.jams.2024.17.2.45</dc:identifier>
  340.    </item>
  341.    <item>
  342.      <title>Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial</title>
  343.      <link>https://pubmed.ncbi.nlm.nih.gov/38686220/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  344.      <description>BACKGROUND: Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD.</description>
  345.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">EClinicalMedicine. 2024 Mar 27;71:102563. doi: 10.1016/j.eclinm.2024.102563. eCollection 2024 May.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. Participants (aged 50-65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. Computer-generated randomisation was done in a 1:1 ratio through permutated-block scheduling. Treatment allocation was concealed for participants and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. Intention-to-treat analysis was performed using a mixed model for repeated measures analysis. This completed trial is registered on ClinicalTrials.gov (NCT03808389).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">FINDINGS: Between December 2020 and December 2021, FMT procedures were conducted on 46 patients with PD: 22 in the healthy donor group and 24 in the placebo group. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 participants in the healthy donor group and 22 in the placebo group. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI -11.4 to -0.2) in the healthy donor group and by 2.7 points (-8.3 to 2.9) in the placebo group (p = 0.0235). Adverse events were limited to temporary abdominal discomfort.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">INTERPRETATION: Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on motor symptoms in patients with early-stage PD. These findings highlight the potential of modulating the gut microbiome as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of patients with PD in various disease stages.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">FUNDING: Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38686220/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38686220</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11056595/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11056595</a> | DOI:<a href=https://doi.org/10.1016/j.eclinm.2024.102563>10.1016/j.eclinm.2024.102563</a></p></div>]]></content:encoded>
  346.      <guid isPermaLink="false">pubmed:38686220</guid>
  347.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  348.      <dc:creator>Arnout Bruggeman</dc:creator>
  349.      <dc:creator>Charysse Vandendriessche</dc:creator>
  350.      <dc:creator>Hannelore Hamerlinck</dc:creator>
  351.      <dc:creator>Danny De Looze</dc:creator>
  352.      <dc:creator>David J Tate</dc:creator>
  353.      <dc:creator>Marnik Vuylsteke</dc:creator>
  354.      <dc:creator>Lindsey De Commer</dc:creator>
  355.      <dc:creator>Lindsay Devolder</dc:creator>
  356.      <dc:creator>Jeroen Raes</dc:creator>
  357.      <dc:creator>Bruno Verhasselt</dc:creator>
  358.      <dc:creator>Debby Laukens</dc:creator>
  359.      <dc:creator>Roosmarijn E Vandenbroucke</dc:creator>
  360.      <dc:creator>Patrick Santens</dc:creator>
  361.      <dc:date>2024-04-30</dc:date>
  362.      <dc:source>EClinicalMedicine</dc:source>
  363.      <dc:title>Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial</dc:title>
  364.      <dc:identifier>pmid:38686220</dc:identifier>
  365.      <dc:identifier>pmc:PMC11056595</dc:identifier>
  366.      <dc:identifier>doi:10.1016/j.eclinm.2024.102563</dc:identifier>
  367.    </item>
  368.    <item>
  369.      <title>Eye Movement Desensitisation and Reprocessing (EMDR) therapy for prolonged grief: theory, research, and practice</title>
  370.      <link>https://pubmed.ncbi.nlm.nih.gov/38686121/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  371.      <description>Prolonged Grief Disorder occurs within 7-10% of the bereaved population and is a more complicated and persistent form of grief which has been associated with suicidality, mental health disorders, sleep disturbance, poor health behaviors, and work and social impairment. EMDR is a fitting treatment option for those with Prolonged Grief, focusing on processing past memories, blocks, current triggers, future fears, and preparing the person for living life beyond the loss in line with the Adaptive...</description>
  372.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Front Psychiatry. 2024 Apr 15;15:1357390. doi: 10.3389/fpsyt.2024.1357390. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Prolonged Grief Disorder occurs within 7-10% of the bereaved population and is a more complicated and persistent form of grief which has been associated with suicidality, mental health disorders, sleep disturbance, poor health behaviors, and work and social impairment. EMDR is a fitting treatment option for those with Prolonged Grief, focusing on processing past memories, blocks, current triggers, future fears, and preparing the person for living life beyond the loss in line with the Adaptive Information Processing Model and grief frameworks. This paper discusses the theory, research regarding the application of EMDR with prolonged grief, and gives insight and guidance to clinicians working in this area including a case example.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38686121/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38686121</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11056564/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11056564</a> | DOI:<a href=https://doi.org/10.3389/fpsyt.2024.1357390>10.3389/fpsyt.2024.1357390</a></p></div>]]></content:encoded>
  373.      <guid isPermaLink="false">pubmed:38686121</guid>
  374.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  375.      <dc:creator>Liam Spicer</dc:creator>
  376.      <dc:date>2024-04-30</dc:date>
  377.      <dc:source>Frontiers in psychiatry</dc:source>
  378.      <dc:title>Eye Movement Desensitisation and Reprocessing (EMDR) therapy for prolonged grief: theory, research, and practice</dc:title>
  379.      <dc:identifier>pmid:38686121</dc:identifier>
  380.      <dc:identifier>pmc:PMC11056564</dc:identifier>
  381.      <dc:identifier>doi:10.3389/fpsyt.2024.1357390</dc:identifier>
  382.    </item>
  383.    <item>
  384.      <title>&lt;em&gt;ATP1A3&lt;/em&gt; Disease Spectrum Includes Paroxysmal Weakness and Encephalopathy Not Triggered by Fever</title>
  385.      <link>https://pubmed.ncbi.nlm.nih.gov/38685976/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  386.      <description>BACKGROUND AND OBJECTIVES: Heterozygous pathogenic variants in ATP1A3, which encodes the catalytic alpha subunit of neuronal Na^(+)/K^(+)-ATPase, cause primarily neurologic disorders with widely variable features that can include episodic movement deficits. One distinctive presentation of ATP1A3-related disease is recurrent fever-triggered encephalopathy. This can occur with generalized weakness and/or ataxia and is described in the literature as relapsing encephalopathy with cerebellar ataxia....</description>
  387.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Neurol Genet. 2024 Apr 25;10(3):e200150. doi: 10.1212/NXG.0000000000200150. eCollection 2024 Jun.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND AND OBJECTIVES: Heterozygous pathogenic variants in <i>ATP1A3</i>, which encodes the catalytic alpha subunit of neuronal Na<sup>+</sup>/K<sup>+</sup>-ATPase, cause primarily neurologic disorders with widely variable features that can include episodic movement deficits. One distinctive presentation of <i>ATP1A3</i>-related disease is recurrent fever-triggered encephalopathy. This can occur with generalized weakness and/or ataxia and is described in the literature as relapsing encephalopathy with cerebellar ataxia. This syndrome displays genotype-phenotype correlation with variants at p.R756 causing temperature sensitivity of ATP1A3. We report clinical and in vitro functional evidence for a similar phenotype not triggered by fever but associated with protein loss-of-function.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We describe the phenotype of an individual with de novo occurrence of a novel heterozygous <i>ATP1A3</i> variant, NM_152296.5:c.388_390delGTG; p.(V130del). We confirmed the pathogenicity of p.V130del by cell survival complementation assay in HEK293 cells and then characterized its functional impact on enzymatic ion transport and extracellular sodium binding by two-electrode voltage clamp electrophysiology in <i>Xenopus</i> oocytes. To determine whether variant enzymes reach the cell surface, we surface-biotinylated oocytes expressing N-tagged ATP1A3.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The proband is a 7-year-old boy who has had 2 lifetime episodes of paroxysmal weakness, encephalopathy, and ataxia not triggered by fever. He had speech regression and intermittent hand tremors after the second episode but otherwise spontaneously recovered after episodes and is at present developmentally appropriate. The p.V130del variant was identified on clinical trio exome sequencing, which did not reveal any other variants possibly associated with the phenotype. p.V130del eliminated ATP1A3 function in cell survival complementation assay. In <i>Xenopus</i> oocytes, p.V130del variant Na<sup>+</sup>/K<sup>+</sup>-ATPases showed complete loss of ion transport activity and marked abnormalities of extracellular Na<sup>+</sup> binding at room temperature. Despite this clear loss-of-function effect, surface biotinylation under the same conditions revealed that p.V130del variant enzymes were still present at the oocyte's cell membrane.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">DISCUSSION: This individual's phenotype expands the clinical spectrum of <i>ATP1A3</i>-related recurrent encephalopathy to include presentations without fever-triggered events. The total loss of ion transport function with p.V130del, despite enzyme presence at the cell membrane, indicates that haploinsufficiency can cause relatively mild phenotypes in <i>ATP1A3</i>-related disease.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685976/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685976</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11057438/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11057438</a> | DOI:<a href=https://doi.org/10.1212/NXG.0000000000200150>10.1212/NXG.0000000000200150</a></p></div>]]></content:encoded>
  388.      <guid isPermaLink="false">pubmed:38685976</guid>
  389.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  390.      <dc:creator>Chetan Immanneni</dc:creator>
  391.      <dc:creator>Daniel Calame</dc:creator>
  392.      <dc:creator>Song Jiao</dc:creator>
  393.      <dc:creator>Lisa T Emrick</dc:creator>
  394.      <dc:creator>Miguel Holmgren</dc:creator>
  395.      <dc:creator>Sho T Yano</dc:creator>
  396.      <dc:date>2024-04-30</dc:date>
  397.      <dc:source>Neurology. Genetics</dc:source>
  398.      <dc:title>&lt;em&gt;ATP1A3&lt;/em&gt; Disease Spectrum Includes Paroxysmal Weakness and Encephalopathy Not Triggered by Fever</dc:title>
  399.      <dc:identifier>pmid:38685976</dc:identifier>
  400.      <dc:identifier>pmc:PMC11057438</dc:identifier>
  401.      <dc:identifier>doi:10.1212/NXG.0000000000200150</dc:identifier>
  402.    </item>
  403.    <item>
  404.      <title>Biallelic Variants of MRPS36 Cause a New Form of Leigh Syndrome</title>
  405.      <link>https://pubmed.ncbi.nlm.nih.gov/38685873/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  406.      <description>CONCLUSIONS: Our findings point to MRPS36 as a new disease gene implicated in Leigh syndrome. The slight elevation of plasma levels of glutamate and glutamine observed in patients with OGDHC deficiency represents a candidate metabolic signature of this neurometabolic disorder. © 2024 International Parkinson and Movement Disorder Society.</description>
  407.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mov Disord. 2024 Apr 30. doi: 10.1002/mds.29795. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: The MRPS36 gene encodes a recently identified component of the 2-oxoglutarate dehydrogenase complex (OGDHC), a key enzyme of the Krebs cycle catalyzing the oxidative decarboxylation of 2-oxoglutarate to succinyl-CoA. Defective OGDHC activity causes a clinically variable metabolic disorder characterized by global developmental delay, severe neurological impairment, liver failure, and early-onset lactic acidosis.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We investigated the molecular cause underlying Leigh syndrome with bilateral striatal necrosis in two siblings through exome sequencing. Functional studies included measurement of the OGDHC enzymatic activity and MRPS36 mRNA levels in fibroblasts, assessment of protein stability in transfected cells, and structural analysis. A literature review was performed to define the etiological and phenotypic spectrum of OGDHC deficiency.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: In the two affected brothers, exome sequencing identified a homozygous nonsense variant (c.283G&gt;T, p.Glu95*) of MRPS36. The variant did not affect transcript processing and stability, nor protein levels, but resulted in a shorter protein lacking nine residues that contribute to the structural and functional organization of the OGDHC complex. OGDHC enzymatic activity was significantly reduced. The review of previously reported cases of OGDHC deficiency supports the association of this enzymatic defect with Leigh phenotypic spectrum and early-onset movement disorder. Slightly elevated plasma levels of glutamate and glutamine were observed in our and literature patients with OGDHC defect.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Our findings point to MRPS36 as a new disease gene implicated in Leigh syndrome. The slight elevation of plasma levels of glutamate and glutamine observed in patients with OGDHC deficiency represents a candidate metabolic signature of this neurometabolic disorder. © 2024 International Parkinson and Movement Disorder Society.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685873/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685873</a> | DOI:<a href=https://doi.org/10.1002/mds.29795>10.1002/mds.29795</a></p></div>]]></content:encoded>
  408.      <guid isPermaLink="false">pubmed:38685873</guid>
  409.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  410.      <dc:creator>Serena Galosi</dc:creator>
  411.      <dc:creator>Cecilia Mancini</dc:creator>
  412.      <dc:creator>Anna Commone</dc:creator>
  413.      <dc:creator>Paolo Calligari</dc:creator>
  414.      <dc:creator>Viviana Caputo</dc:creator>
  415.      <dc:creator>Francesca Nardecchia</dc:creator>
  416.      <dc:creator>Claudia Carducci</dc:creator>
  417.      <dc:creator>Lambertus P van den Heuvel</dc:creator>
  418.      <dc:creator>Simone Pizzi</dc:creator>
  419.      <dc:creator>Alessandro Bruselles</dc:creator>
  420.      <dc:creator>Marcello Niceta</dc:creator>
  421.      <dc:creator>Simone Martinelli</dc:creator>
  422.      <dc:creator>Richard J Rodenburg</dc:creator>
  423.      <dc:creator>Marco Tartaglia</dc:creator>
  424.      <dc:creator>Vincenzo Leuzzi</dc:creator>
  425.      <dc:date>2024-04-30</dc:date>
  426.      <dc:source>Movement disorders : official journal of the Movement Disorder Society</dc:source>
  427.      <dc:title>Biallelic Variants of MRPS36 Cause a New Form of Leigh Syndrome</dc:title>
  428.      <dc:identifier>pmid:38685873</dc:identifier>
  429.      <dc:identifier>doi:10.1002/mds.29795</dc:identifier>
  430.    </item>
  431.    <item>
  432.      <title>Letter of response to "concerns about efficacy of deep brain stimulation (DBS) in centromedian-parafascicular thalamic complex for rapid onset dystonia-parkinsonism (DYT12-ATP1A3)"</title>
  433.      <link>https://pubmed.ncbi.nlm.nih.gov/38685262/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  434.      <description>No abstract</description>
  435.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Brain Stimul. 2024 Mar-Apr;17(2):493-495. doi: 10.1016/j.brs.2024.02.015. Epub 2024 Apr 27.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685262/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685262</a> | DOI:<a href=https://doi.org/10.1016/j.brs.2024.02.015>10.1016/j.brs.2024.02.015</a></p></div>]]></content:encoded>
  436.      <guid isPermaLink="false">pubmed:38685262</guid>
  437.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  438.      <dc:creator>Kai-Liang Wang</dc:creator>
  439.      <dc:creator>Ji-Ping Li</dc:creator>
  440.      <dc:creator>Yong-Zhi Shan</dc:creator>
  441.      <dc:creator>Guo-Guang Zhao</dc:creator>
  442.      <dc:creator>Jing-Hong Ma</dc:creator>
  443.      <dc:creator>Adolfo Ramirez-Zamora</dc:creator>
  444.      <dc:creator>Yu-Qing Zhang</dc:creator>
  445.      <dc:date>2024-04-30</dc:date>
  446.      <dc:source>Brain stimulation</dc:source>
  447.      <dc:title>Letter of response to "concerns about efficacy of deep brain stimulation (DBS) in centromedian-parafascicular thalamic complex for rapid onset dystonia-parkinsonism (DYT12-ATP1A3)"</dc:title>
  448.      <dc:identifier>pmid:38685262</dc:identifier>
  449.      <dc:identifier>doi:10.1016/j.brs.2024.02.015</dc:identifier>
  450.    </item>
  451.    <item>
  452.      <title>Concerns about efficacy of deep brain stimulation (DBS) in centromedian-parafascicular thalamic complex for rapid onset dystonia-parkinsonism (DYT12-ATP1A3)</title>
  453.      <link>https://pubmed.ncbi.nlm.nih.gov/38685261/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  454.      <description>No abstract</description>
  455.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Brain Stimul. 2024 Mar-Apr;17(2):491-492. doi: 10.1016/j.brs.2024.02.008. Epub 2024 Apr 27.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685261/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685261</a> | DOI:<a href=https://doi.org/10.1016/j.brs.2024.02.008>10.1016/j.brs.2024.02.008</a></p></div>]]></content:encoded>
  456.      <guid isPermaLink="false">pubmed:38685261</guid>
  457.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  458.      <dc:creator>Laura Cif</dc:creator>
  459.      <dc:creator>Mayté Castro Jimenez</dc:creator>
  460.      <dc:creator>Julien F Bally</dc:creator>
  461.      <dc:date>2024-04-30</dc:date>
  462.      <dc:source>Brain stimulation</dc:source>
  463.      <dc:title>Concerns about efficacy of deep brain stimulation (DBS) in centromedian-parafascicular thalamic complex for rapid onset dystonia-parkinsonism (DYT12-ATP1A3)</dc:title>
  464.      <dc:identifier>pmid:38685261</dc:identifier>
  465.      <dc:identifier>doi:10.1016/j.brs.2024.02.008</dc:identifier>
  466.    </item>
  467.    <item>
  468.      <title>Pre-existing oscillatory activity as a condition for sub-harmonic entrainment of finely tuned gamma in Parkinson's disease</title>
  469.      <link>https://pubmed.ncbi.nlm.nih.gov/38685260/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  470.      <description>No abstract</description>
  471.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Brain Stimul. 2024 Mar-Apr;17(2):488-490. doi: 10.1016/j.brs.2024.02.017. Epub 2024 Apr 27.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685260/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685260</a> | DOI:<a href=https://doi.org/10.1016/j.brs.2024.02.017>10.1016/j.brs.2024.02.017</a></p></div>]]></content:encoded>
  472.      <guid isPermaLink="false">pubmed:38685260</guid>
  473.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  474.      <dc:creator>James J Sermon</dc:creator>
  475.      <dc:creator>Philip A Starr</dc:creator>
  476.      <dc:creator>Timothy Denison</dc:creator>
  477.      <dc:creator>Benoit Duchet</dc:creator>
  478.      <dc:date>2024-04-30</dc:date>
  479.      <dc:source>Brain stimulation</dc:source>
  480.      <dc:title>Pre-existing oscillatory activity as a condition for sub-harmonic entrainment of finely tuned gamma in Parkinson's disease</dc:title>
  481.      <dc:identifier>pmid:38685260</dc:identifier>
  482.      <dc:identifier>doi:10.1016/j.brs.2024.02.017</dc:identifier>
  483.    </item>
  484.    <item>
  485.      <title>A phenomenological model of deep brain stimulation induced finely tuned gamma oscillations in the subthalamic nucleus</title>
  486.      <link>https://pubmed.ncbi.nlm.nih.gov/38685259/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  487.      <description>No abstract</description>
  488.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Brain Stimul. 2024 Mar-Apr;17(2):485-487. doi: 10.1016/j.brs.2023.12.004. Epub 2024 Apr 27.</p><p><b>NO ABSTRACT</b></p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685259/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685259</a> | DOI:<a href=https://doi.org/10.1016/j.brs.2023.12.004>10.1016/j.brs.2023.12.004</a></p></div>]]></content:encoded>
  489.      <guid isPermaLink="false">pubmed:38685259</guid>
  490.      <pubDate>Tue, 30 Apr 2024 06:00:00 -0400</pubDate>
  491.      <dc:creator>M Scherer</dc:creator>
  492.      <dc:creator>D Crompton</dc:creator>
  493.      <dc:creator>L Milosevic</dc:creator>
  494.      <dc:date>2024-04-30</dc:date>
  495.      <dc:source>Brain stimulation</dc:source>
  496.      <dc:title>A phenomenological model of deep brain stimulation induced finely tuned gamma oscillations in the subthalamic nucleus</dc:title>
  497.      <dc:identifier>pmid:38685259</dc:identifier>
  498.      <dc:identifier>doi:10.1016/j.brs.2023.12.004</dc:identifier>
  499.    </item>
  500.    <item>
  501.      <title>imply: improving cell-type deconvolution accuracy using personalized reference profiles</title>
  502.      <link>https://pubmed.ncbi.nlm.nih.gov/38685057/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  503.      <description>Using computational tools, bulk transcriptomics can be deconvoluted to estimate the abundance of constituent cell types. However, existing deconvolution methods are conditioned on the assumption that the whole study population is served by a single reference panel, ignoring person-to-person heterogeneity. Here, we present imply, a novel algorithm to deconvolute cell type proportions using personalized reference panels. Simulation studies demonstrate reduced bias compared with existing methods....</description>
  504.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Genome Med. 2024 Apr 29;16(1):65. doi: 10.1186/s13073-024-01338-z.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Using computational tools, bulk transcriptomics can be deconvoluted to estimate the abundance of constituent cell types. However, existing deconvolution methods are conditioned on the assumption that the whole study population is served by a single reference panel, ignoring person-to-person heterogeneity. Here, we present imply, a novel algorithm to deconvolute cell type proportions using personalized reference panels. Simulation studies demonstrate reduced bias compared with existing methods. Real data analyses on longitudinal consortia show disparities in cell type proportions are associated with several disease phenotypes in Type 1 diabetes and Parkinson's disease. imply is available through the R/Bioconductor package ISLET at https://bioconductor.org/packages/ISLET/ .</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38685057/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38685057</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11057104/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11057104</a> | DOI:<a href=https://doi.org/10.1186/s13073-024-01338-z>10.1186/s13073-024-01338-z</a></p></div>]]></content:encoded>
  505.      <guid isPermaLink="false">pubmed:38685057</guid>
  506.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  507.      <dc:creator>Guanqun Meng</dc:creator>
  508.      <dc:creator>Yue Pan</dc:creator>
  509.      <dc:creator>Wen Tang</dc:creator>
  510.      <dc:creator>Lijun Zhang</dc:creator>
  511.      <dc:creator>Ying Cui</dc:creator>
  512.      <dc:creator>Fredrick R Schumacher</dc:creator>
  513.      <dc:creator>Ming Wang</dc:creator>
  514.      <dc:creator>Rui Wang</dc:creator>
  515.      <dc:creator>Sijia He</dc:creator>
  516.      <dc:creator>Jeffrey Krischer</dc:creator>
  517.      <dc:creator>Qian Li</dc:creator>
  518.      <dc:creator>Hao Feng</dc:creator>
  519.      <dc:date>2024-04-29</dc:date>
  520.      <dc:source>Genome medicine</dc:source>
  521.      <dc:title>imply: improving cell-type deconvolution accuracy using personalized reference profiles</dc:title>
  522.      <dc:identifier>pmid:38685057</dc:identifier>
  523.      <dc:identifier>pmc:PMC11057104</dc:identifier>
  524.      <dc:identifier>doi:10.1186/s13073-024-01338-z</dc:identifier>
  525.    </item>
  526.    <item>
  527.      <title>Protocol for combined N-of-1 trials to assess cerebellar neurostimulation for movement disorders in children and young adults with dyskinetic cerebral palsy</title>
  528.      <link>https://pubmed.ncbi.nlm.nih.gov/38684956/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  529.      <description>BACKGROUND: Movement and tone disorders in children and young adults with cerebral palsy are a great source of disability. Deep brain stimulation (DBS) of basal ganglia targets has a major role in the treatment of isolated dystonias, but its efficacy in dyskinetic cerebral palsy (DCP) is lower, due to structural basal ganglia and thalamic damage and lack of improvement of comorbid choreoathetosis and spasticity. The cerebellum is an attractive target for DBS in DCP since it is frequently spared...</description>
  530.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMC Neurol. 2024 Apr 29;24(1):145. doi: 10.1186/s12883-024-03633-z.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Movement and tone disorders in children and young adults with cerebral palsy are a great source of disability. Deep brain stimulation (DBS) of basal ganglia targets has a major role in the treatment of isolated dystonias, but its efficacy in dyskinetic cerebral palsy (DCP) is lower, due to structural basal ganglia and thalamic damage and lack of improvement of comorbid choreoathetosis and spasticity. The cerebellum is an attractive target for DBS in DCP since it is frequently spared from hypoxic ischemic damage, it has a significant role in dystonia network models, and small studies have shown promise of dentate stimulation in improving CP-related movement and tone disorders.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Ten children and young adults with DCP and disabling movement disorders with or without spasticity will undergo bilateral DBS in the dorsal dentate nucleus, with the most distal contact ending in the superior cerebellar peduncle. We will implant Medtronic Percept, a bidirectional neurostimulator that can sense and store brain activity and deliver DBS therapy. The efficacy of cerebellar DBS in improving quality of life and motor outcomes will be tested by a series of N-of-1 clinical trials. Each N-of-1 trial will consist of three blocks, each consisting of one month of effective stimulation and one month of sham stimulation in a random order with weekly motor and quality of life scales as primary and secondary outcomes. In addition, we will characterize abnormal patterns of cerebellar oscillatory activity measured by local field potentials from the intracranial electrodes related to clinical assessments and wearable monitors. Pre- and 12-month postoperative volumetric structural and functional MRI and diffusion tensor imaging will be used to identify candidate imaging markers of baseline disease severity and response to DBS.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">DISCUSSION: Our goal is to test a cerebellar neuromodulation therapy that produces meaningful changes in function and well-being for people with CP, obtain a mechanistic understanding of the underlying brain network disorder, and identify physiological and imaging-based predictors of outcomes useful in planning further studies.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">TRIAL REGISTRATION: ClinicalTrials.gov NCT06122675, first registered November 7, 2023.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38684956/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38684956</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11057158/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11057158</a> | DOI:<a href=https://doi.org/10.1186/s12883-024-03633-z>10.1186/s12883-024-03633-z</a></p></div>]]></content:encoded>
  531.      <guid isPermaLink="false">pubmed:38684956</guid>
  532.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  533.      <dc:creator>M San Luciano</dc:creator>
  534.      <dc:creator>C R Oehrn</dc:creator>
  535.      <dc:creator>S S Wang</dc:creator>
  536.      <dc:creator>J S Tolmie</dc:creator>
  537.      <dc:creator>A Wiltshire</dc:creator>
  538.      <dc:creator>R E Graff</dc:creator>
  539.      <dc:creator>J Zhu</dc:creator>
  540.      <dc:creator>P A Starr</dc:creator>
  541.      <dc:date>2024-04-29</dc:date>
  542.      <dc:source>BMC neurology</dc:source>
  543.      <dc:title>Protocol for combined N-of-1 trials to assess cerebellar neurostimulation for movement disorders in children and young adults with dyskinetic cerebral palsy</dc:title>
  544.      <dc:identifier>pmid:38684956</dc:identifier>
  545.      <dc:identifier>pmc:PMC11057158</dc:identifier>
  546.      <dc:identifier>doi:10.1186/s12883-024-03633-z</dc:identifier>
  547.    </item>
  548.    <item>
  549.      <title>Resveratrol and 1,25-dihydroxyvitamin D decrease Lingo-1 levels, and improve behavior in harmaline-induced Essential tremor, suggesting potential therapeutic benefits</title>
  550.      <link>https://pubmed.ncbi.nlm.nih.gov/38684734/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  551.      <description>Essential tremor (ET) is a neurological disease that impairs motor and cognitive functioning. A variant of the Lingo-1 genetic locus is associated with a heightened ET risk, and increased expression of cerebellar Lingo-1. Lingo-1 has been associated with neurodegenerative processes; however, neuroprotection from ET-associated degeneration can be conferred by the protein Sirt1. Sirt1 activity can be promoted by Resveratrol (Res) and 1,25-dihydroxyvitamin D3 (VitD3), and thus these factors may...</description>
  552.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Sci Rep. 2024 Apr 29;14(1):9864. doi: 10.1038/s41598-024-60518-4.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Essential tremor (ET) is a neurological disease that impairs motor and cognitive functioning. A variant of the Lingo-1 genetic locus is associated with a heightened ET risk, and increased expression of cerebellar Lingo-1. Lingo-1 has been associated with neurodegenerative processes; however, neuroprotection from ET-associated degeneration can be conferred by the protein Sirt1. Sirt1 activity can be promoted by Resveratrol (Res) and 1,25-dihydroxyvitamin D3 (VitD3), and thus these factors may exert neuroprotective properties through a Sirt1 mechanism. As Res and VitD3 are linked to Sirt1, enhancing Sirt1 could counteract the negative effects of increased Lingo-1. Therefore, we hypothesized that a combination of Res-VitD3 in a harmaline injection model of ET would modulate Sirt1 and Lingo-1 levels. As expected, harmaline exposure (10 mg/kg/every other day; i.p.) impaired motor coordination, enhanced tremors, rearing, and cognitive dysfunction. When Res (5 mg/kg/day; i.p.) and VitD3 (0.1 mg/kg/day; i.p.) were given to adult rats (n = 8 per group) an hour before harmaline, tremor severity, rearing, and memory impairment were reduced. Individual treatment with Res and VitD3 decreased Lingo-1 gene expression levels in qPCR assays. Co-treatment with Res and VitD3 increased and decreased Sirt1 and Lingo-1 gene expression levels, respectively, and in some cases, beneficial effects on behavior were noted, which were not seen when Res or VitD3 were individually applied. Taken together, our study found that Res and VitD3 improved locomotor and cognitive deficits, modulated Sirt1 and Lingo-1. Therefore, we would recommend co-treatment of VitD3 and Res to leverage complementary effects for the management of ET symptoms.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38684734/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38684734</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11058818/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11058818</a> | DOI:<a href=https://doi.org/10.1038/s41598-024-60518-4>10.1038/s41598-024-60518-4</a></p></div>]]></content:encoded>
  553.      <guid isPermaLink="false">pubmed:38684734</guid>
  554.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  555.      <dc:creator>Zeynab Pirmoradi</dc:creator>
  556.      <dc:creator>Mohsen Nakhaie</dc:creator>
  557.      <dc:creator>Hoda Ranjbar</dc:creator>
  558.      <dc:creator>Davood Kalantar-Neyestanaki</dc:creator>
  559.      <dc:creator>Kristi A Kohlmeier</dc:creator>
  560.      <dc:creator>Majid Asadi-Shekaari</dc:creator>
  561.      <dc:creator>Amin Hassanshahi</dc:creator>
  562.      <dc:creator>Mohammad Shabani</dc:creator>
  563.      <dc:date>2024-04-29</dc:date>
  564.      <dc:source>Scientific reports</dc:source>
  565.      <dc:title>Resveratrol and 1,25-dihydroxyvitamin D decrease Lingo-1 levels, and improve behavior in harmaline-induced Essential tremor, suggesting potential therapeutic benefits</dc:title>
  566.      <dc:identifier>pmid:38684734</dc:identifier>
  567.      <dc:identifier>pmc:PMC11058818</dc:identifier>
  568.      <dc:identifier>doi:10.1038/s41598-024-60518-4</dc:identifier>
  569.    </item>
  570.    <item>
  571.      <title>Mitochondrial complex I deficiency stratifies idiopathic Parkinson's disease</title>
  572.      <link>https://pubmed.ncbi.nlm.nih.gov/38684731/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  573.      <description>Idiopathic Parkinson's disease (iPD) is believed to have a heterogeneous pathophysiology, but molecular disease subtypes have not been identified. Here, we show that iPD can be stratified according to the severity of neuronal respiratory complex I (CI) deficiency, and identify two emerging disease subtypes with distinct molecular and clinical profiles. The CI deficient (CI-PD) subtype accounts for approximately a fourth of all cases, and is characterized by anatomically widespread neuronal CI...</description>
  574.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Nat Commun. 2024 Apr 29;15(1):3631. doi: 10.1038/s41467-024-47867-4.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Idiopathic Parkinson's disease (iPD) is believed to have a heterogeneous pathophysiology, but molecular disease subtypes have not been identified. Here, we show that iPD can be stratified according to the severity of neuronal respiratory complex I (CI) deficiency, and identify two emerging disease subtypes with distinct molecular and clinical profiles. The CI deficient (CI-PD) subtype accounts for approximately a fourth of all cases, and is characterized by anatomically widespread neuronal CI deficiency, a distinct cell type-specific gene expression profile, increased load of neuronal mtDNA deletions, and a predilection for non-tremor dominant motor phenotypes. In contrast, the non-CI deficient (nCI-PD) subtype exhibits no evidence of mitochondrial impairment outside the dopaminergic substantia nigra and has a predilection for a tremor dominant phenotype. These findings constitute a step towards resolving the biological heterogeneity of iPD with implications for both mechanistic understanding and treatment strategies.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38684731/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38684731</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11059185/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11059185</a> | DOI:<a href=https://doi.org/10.1038/s41467-024-47867-4>10.1038/s41467-024-47867-4</a></p></div>]]></content:encoded>
  575.      <guid isPermaLink="false">pubmed:38684731</guid>
  576.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  577.      <dc:creator>Irene H Flønes</dc:creator>
  578.      <dc:creator>Lilah Toker</dc:creator>
  579.      <dc:creator>Dagny Ann Sandnes</dc:creator>
  580.      <dc:creator>Martina Castelli</dc:creator>
  581.      <dc:creator>Sepideh Mostafavi</dc:creator>
  582.      <dc:creator>Njål Lura</dc:creator>
  583.      <dc:creator>Omnia Shadad</dc:creator>
  584.      <dc:creator>Erika Fernandez-Vizarra</dc:creator>
  585.      <dc:creator>Cèlia Painous</dc:creator>
  586.      <dc:creator>Alexandra Pérez-Soriano</dc:creator>
  587.      <dc:creator>Yaroslau Compta</dc:creator>
  588.      <dc:creator>Laura Molina-Porcel</dc:creator>
  589.      <dc:creator>Guido Alves</dc:creator>
  590.      <dc:creator>Ole-Bjørn Tysnes</dc:creator>
  591.      <dc:creator>Christian Dölle</dc:creator>
  592.      <dc:creator>Gonzalo S Nido</dc:creator>
  593.      <dc:creator>Charalampos Tzoulis</dc:creator>
  594.      <dc:date>2024-04-29</dc:date>
  595.      <dc:source>Nature communications</dc:source>
  596.      <dc:title>Mitochondrial complex I deficiency stratifies idiopathic Parkinson's disease</dc:title>
  597.      <dc:identifier>pmid:38684731</dc:identifier>
  598.      <dc:identifier>pmc:PMC11059185</dc:identifier>
  599.      <dc:identifier>doi:10.1038/s41467-024-47867-4</dc:identifier>
  600.    </item>
  601.    <item>
  602.      <title>Investigation of the nonmotor symptoms in patients with STN-DBS therapy in comparison with those without STN-DBS</title>
  603.      <link>https://pubmed.ncbi.nlm.nih.gov/38684577/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  604.      <description>The impact of STN-DBS on NMS remains rather as an underestimated topic. Besides, the significance of NMSs in QOL indexes of PD subjects with STN-DBS is unknown. We primarily aimed to evaluate the NMSs and their significance in QOL indexes in PD subjects comparatively with and without STN-DBS therapy. We enrolled all consecutive PD subjects with and without STN-DBS who applied to our movement disorders outpatient clinics between January/2023 and September/2023. We performed comprehensive...</description>
  605.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Neural Transm (Vienna). 2024 Apr 30. doi: 10.1007/s00702-024-02778-y. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">The impact of STN-DBS on NMS remains rather as an underestimated topic. Besides, the significance of NMSs in QOL indexes of PD subjects with STN-DBS is unknown. We primarily aimed to evaluate the NMSs and their significance in QOL indexes in PD subjects comparatively with and without STN-DBS therapy. We enrolled all consecutive PD subjects with and without STN-DBS who applied to our movement disorders outpatient clinics between January/2023 and September/2023. We performed comprehensive assessments of the motor and nonmotor features including the clinical scales of Movement Disorder Society-sponsored revision of the MDS-UPDRS, NMSS, HAM-A, HAM-D, and the PDQ-39. Overall, 48 PD subjects with STN-DBS and 161 without STN-DBS treatment were included. The comparative analyses revealed that the sub-scores of the MDS-UPDRS-2, -3 and -4 were higher in the STN-DBS group. However, the MDS-UDPRS-1 and the total scores of the NMSS were similar between groups. Among eight subitems of the NMSS, only, the sub scores of the mood/cognition and the gastrointestinal tract differed. Remarkably, the significant correlations between the scores of the QOL and the NMSS scores in the STN-DBS (-) group, did not persist within the STN-DBS group. Remarkably, the correlations between the NMSS and PQQ-39 disappeared for most of the sub scores within the STN-DBS group. We found indirect evidence regarding the benefit of STN-DBS therapy on NMSs in our cross-sectional study. Besides, we found weaker impact of NMSs in QOL indexes in PD subjects with STN-DBS therapy.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38684577/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38684577</a> | DOI:<a href=https://doi.org/10.1007/s00702-024-02778-y>10.1007/s00702-024-02778-y</a></p></div>]]></content:encoded>
  606.      <guid isPermaLink="false">pubmed:38684577</guid>
  607.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  608.      <dc:creator>Halil Onder</dc:creator>
  609.      <dc:creator>Selcuk Comoglu</dc:creator>
  610.      <dc:date>2024-04-29</dc:date>
  611.      <dc:source>Journal of neural transmission (Vienna, Austria : 1996)</dc:source>
  612.      <dc:title>Investigation of the nonmotor symptoms in patients with STN-DBS therapy in comparison with those without STN-DBS</dc:title>
  613.      <dc:identifier>pmid:38684577</dc:identifier>
  614.      <dc:identifier>doi:10.1007/s00702-024-02778-y</dc:identifier>
  615.    </item>
  616.    <item>
  617.      <title>Oculomasticatory rhythmic movements, insomnia and stroke-like episodes in a patient with POLG mutation</title>
  618.      <link>https://pubmed.ncbi.nlm.nih.gov/38684350/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  619.      <description>The POLG mutation, a leading cause of mitochondrial diseases, exhibits a wide-ranging age of onset and a complex clinical presentation. We encountered an atypical clinical profile in an elderly man with a POLG mutation, characterised by a stroke-like episode, chronic insomnia and transient oculomasticatory rhythmic movement. History revealed chronic constipation since his 50s and progressive bilateral ophthalmoplegia since his early 60s. Subsequently, he had experienced acute encephalopathy and...</description>
  620.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">BMJ Case Rep. 2024 Apr 29;17(4):e259426. doi: 10.1136/bcr-2023-259426.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">The POLG mutation, a leading cause of mitochondrial diseases, exhibits a wide-ranging age of onset and a complex clinical presentation. We encountered an atypical clinical profile in an elderly man with a POLG mutation, characterised by a stroke-like episode, chronic insomnia and transient oculomasticatory rhythmic movement. History revealed chronic constipation since his 50s and progressive bilateral ophthalmoplegia since his early 60s. Subsequently, he had experienced acute encephalopathy and later developed chronic insomnia. The present neurological examination showed bilateral complete ophthalmoplegia, ptosis, and rhythmic ocular and jaw movements. Imaging indicated findings suggestive of a stroke-like episode and eventual genetic analysis revealed a homozygous missense mutation in the POLG gene. This case expands the clinical spectrum of POLG mutations in individuals over 60 years, showcasing the rare combination of a stroke-like episode, chronic insomnia and oculomasticatory rhythmic movement.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38684350/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38684350</a> | DOI:<a href=https://doi.org/10.1136/bcr-2023-259426>10.1136/bcr-2023-259426</a></p></div>]]></content:encoded>
  621.      <guid isPermaLink="false">pubmed:38684350</guid>
  622.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  623.      <dc:creator>Rithvik Ramesh</dc:creator>
  624.      <dc:creator>Chitneni Amanmahanya</dc:creator>
  625.      <dc:creator>Vengadakrishnan Krishnamoorthy</dc:creator>
  626.      <dc:creator>Vasanthan Krishnan</dc:creator>
  627.      <dc:creator>Sathyamoorthy Palani</dc:creator>
  628.      <dc:creator>Lakshmi Narasimhan Ranganathan</dc:creator>
  629.      <dc:date>2024-04-29</dc:date>
  630.      <dc:source>BMJ case reports</dc:source>
  631.      <dc:title>Oculomasticatory rhythmic movements, insomnia and stroke-like episodes in a patient with POLG mutation</dc:title>
  632.      <dc:identifier>pmid:38684350</dc:identifier>
  633.      <dc:identifier>doi:10.1136/bcr-2023-259426</dc:identifier>
  634.    </item>
  635.    <item>
  636.      <title>Human mutations in high-confidence Tourette disorder genes affect sensorimotor behavior, reward learning, and striatal dopamine in mice</title>
  637.      <link>https://pubmed.ncbi.nlm.nih.gov/38683996/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  638.      <description>Tourette disorder (TD) is poorly understood, despite affecting 1/160 children. A lack of animal models possessing construct, face, and predictive validity hinders progress in the field. We used CRISPR/Cas9 genome editing to generate mice with mutations orthologous to human de novo variants in two high-confidence Tourette genes, CELSR3 and WWC1. Mice with human mutations in Celsr3 and Wwc1 exhibit cognitive and/or sensorimotor behavioral phenotypes consistent with TD. Sensorimotor gating...</description>
  639.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Proc Natl Acad Sci U S A. 2024 May 7;121(19):e2307156121. doi: 10.1073/pnas.2307156121. Epub 2024 Apr 29.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Tourette disorder (TD) is poorly understood, despite affecting 1/160 children. A lack of animal models possessing construct, face, and predictive validity hinders progress in the field. We used CRISPR/Cas9 genome editing to generate mice with mutations orthologous to human de novo variants in two high-confidence Tourette genes, <i>CELSR3</i> and <i>WWC1</i>. Mice with human mutations in <i>Celsr3</i> and <i>Wwc1</i> exhibit cognitive and/or sensorimotor behavioral phenotypes consistent with TD. Sensorimotor gating deficits, as measured by acoustic prepulse inhibition, occur in both male and female <i>Celsr3</i> TD models. <i>Wwc1</i> mice show reduced prepulse inhibition only in females. Repetitive motor behaviors, common to <i>Celsr3</i> mice and more pronounced in females, include vertical rearing and grooming. Sensorimotor gating deficits and rearing are attenuated by aripiprazole, a partial agonist at dopamine type II receptors. Unsupervised machine learning reveals numerous changes to spontaneous motor behavior and less predictable patterns of movement. Continuous fixed-ratio reinforcement shows that <i>Celsr3</i> TD mice have enhanced motor responding and reward learning. Electrically evoked striatal dopamine release, tested in one model, is greater. Brain development is otherwise grossly normal without signs of striatal interneuron loss. Altogether, mice expressing human mutations in high-confidence TD genes exhibit face and predictive validity. Reduced prepulse inhibition and repetitive motor behaviors are core behavioral phenotypes and are responsive to aripiprazole. Enhanced reward learning and motor responding occur alongside greater evoked dopamine release. Phenotypes can also vary by sex and show stronger affection in females, an unexpected finding considering males are more frequently affected in TD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38683996/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38683996</a> | DOI:<a href=https://doi.org/10.1073/pnas.2307156121>10.1073/pnas.2307156121</a></p></div>]]></content:encoded>
  640.      <guid isPermaLink="false">pubmed:38683996</guid>
  641.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  642.      <dc:creator>Cara Nasello</dc:creator>
  643.      <dc:creator>Lauren A Poppi</dc:creator>
  644.      <dc:creator>Junbing Wu</dc:creator>
  645.      <dc:creator>Tess F Kowalski</dc:creator>
  646.      <dc:creator>Joshua K Thackray</dc:creator>
  647.      <dc:creator>Riley Wang</dc:creator>
  648.      <dc:creator>Angelina Persaud</dc:creator>
  649.      <dc:creator>Mariam Mahboob</dc:creator>
  650.      <dc:creator>Sherry Lin</dc:creator>
  651.      <dc:creator>Rodna Spaseska</dc:creator>
  652.      <dc:creator>C K Johnson</dc:creator>
  653.      <dc:creator>Derek Gordon</dc:creator>
  654.      <dc:creator>Fadel Tissir</dc:creator>
  655.      <dc:creator>Gary A Heiman</dc:creator>
  656.      <dc:creator>Jay A Tischfield</dc:creator>
  657.      <dc:creator>Miriam Bocarsly</dc:creator>
  658.      <dc:creator>Max A Tischfield</dc:creator>
  659.      <dc:date>2024-04-29</dc:date>
  660.      <dc:source>Proceedings of the National Academy of Sciences of the United States of America</dc:source>
  661.      <dc:title>Human mutations in high-confidence Tourette disorder genes affect sensorimotor behavior, reward learning, and striatal dopamine in mice</dc:title>
  662.      <dc:identifier>pmid:38683996</dc:identifier>
  663.      <dc:identifier>doi:10.1073/pnas.2307156121</dc:identifier>
  664.    </item>
  665.    <item>
  666.      <title>Safranal exerts a neuroprotective effect on Parkinson's disease with suppression of NLRP3 inflammation activation</title>
  667.      <link>https://pubmed.ncbi.nlm.nih.gov/38683404/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  668.      <description>CONCLUSIONS: Safranal played a neuroprotective effect on the Parkinson's disease and its mechanism was related to the inhibition of NLRP3 inflammasome activation.</description>
  669.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mol Biol Rep. 2024 Apr 29;51(1):593. doi: 10.1007/s11033-024-09537-y.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Parkinson's disease (PD) is a common central nervous system neurodegenerative disease. Neuroinflammation is one of the significant neuropathological hallmarks. As a traditional Chinese medicine, Safranal exerts anti-inflammatory effects in various diseases, however, whether it plays a similar effect on PD is still unclear. The study was to investigate the effects and mechanism of Safranal on PD.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: The PD mouse model was established by 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine MPTP firstly. Next, the degree of muscle stiffness, neuromuscular function, motor retardation and motor coordination ability were examined by observing and testing mouse movement behavior. Immunofluorescence staining was used to observe the expression of tyrosine hydroxylase (TH). The dopamine (DA) content of the striatum was detected by High-performance liquid chromatography (HPLC). The expression of TH and NLRP3 inflammasome-related markers NLRP3, IL-1β, and Capase-1 were detected by Real-time Polymerase Chain Reaction (qRT-PCR) and western blotting (WB) respectively.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Through behavioral testing, Parkinson's mouse showed a higher muscle stiffness and neuromuscular tension, a more motor retardation and activity disorders, together with a worse motor coordination compared with sham group. Simultaneously, DA content and TH expression in the striatum were decreased. However, after using Safranal treatment, the above pathological symptoms of Parkinson's mouse all improved compared with Safranal untreated group, the DA content and TH expression were also increased to varying degrees. Surprisingly, it observed a suppression of NLRP3 inflammation in the striatum of Parkinson's mouse.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Safranal played a neuroprotective effect on the Parkinson's disease and its mechanism was related to the inhibition of NLRP3 inflammasome activation.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38683404/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38683404</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11059006/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11059006</a> | DOI:<a href=https://doi.org/10.1007/s11033-024-09537-y>10.1007/s11033-024-09537-y</a></p></div>]]></content:encoded>
  670.      <guid isPermaLink="false">pubmed:38683404</guid>
  671.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  672.      <dc:creator>Wenping Yang</dc:creator>
  673.      <dc:creator>Yongyue Wei</dc:creator>
  674.      <dc:creator>Jin Sun</dc:creator>
  675.      <dc:creator>Caixia Yao</dc:creator>
  676.      <dc:creator>Fen Ai</dc:creator>
  677.      <dc:creator>Haixia Ding</dc:creator>
  678.      <dc:date>2024-04-29</dc:date>
  679.      <dc:source>Molecular biology reports</dc:source>
  680.      <dc:title>Safranal exerts a neuroprotective effect on Parkinson's disease with suppression of NLRP3 inflammation activation</dc:title>
  681.      <dc:identifier>pmid:38683404</dc:identifier>
  682.      <dc:identifier>pmc:PMC11059006</dc:identifier>
  683.      <dc:identifier>doi:10.1007/s11033-024-09537-y</dc:identifier>
  684.    </item>
  685.    <item>
  686.      <title>Interplay between α-synuclein and parkin genes: Insights of Parkinson's disease</title>
  687.      <link>https://pubmed.ncbi.nlm.nih.gov/38683365/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  688.      <description>Parkinson's disease (PD) is a complex and debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra. The pathogenesis of PD is intimately linked to the roles of two key molecular players, α-synuclein (α-syn) and Parkin. Understanding the intricate interplay between α-syn and Parkin is essential for unravelling the molecular underpinnings of PD. Their roles in synaptic function and protein quality control underscore their...</description>
  689.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Mol Biol Rep. 2024 Apr 29;51(1):586. doi: 10.1007/s11033-024-09520-7.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Parkinson's disease (PD) is a complex and debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra. The pathogenesis of PD is intimately linked to the roles of two key molecular players, α-synuclein (α-syn) and Parkin. Understanding the intricate interplay between α-syn and Parkin is essential for unravelling the molecular underpinnings of PD. Their roles in synaptic function and protein quality control underscore their significance in neuronal health. Dysregulation of these processes, as seen in PD, highlights the potential for targeted therapeutic strategies aimed at restoring normal protein homeostasis and mitigating neurodegeneration. Investigating the connections between α-syn, Parkin, and various pathological mechanisms provides insights into the complex web of factors contributing to PD pathogenesis and offers hope for the development of more effective treatments for this devastating neurological disorder. The present compilation provides an overview of their structures, regional and cellular locations, associations, physiological functions, and pathological roles in the context of PD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38683365/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38683365</a> | DOI:<a href=https://doi.org/10.1007/s11033-024-09520-7>10.1007/s11033-024-09520-7</a></p></div>]]></content:encoded>
  690.      <guid isPermaLink="false">pubmed:38683365</guid>
  691.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  692.      <dc:creator>Kajal Sharma</dc:creator>
  693.      <dc:creator>Shivani Chib</dc:creator>
  694.      <dc:creator>Aniket Gupta</dc:creator>
  695.      <dc:creator>Randhir Singh</dc:creator>
  696.      <dc:creator>Rishabh Chalotra</dc:creator>
  697.      <dc:date>2024-04-29</dc:date>
  698.      <dc:source>Molecular biology reports</dc:source>
  699.      <dc:title>Interplay between α-synuclein and parkin genes: Insights of Parkinson's disease</dc:title>
  700.      <dc:identifier>pmid:38683365</dc:identifier>
  701.      <dc:identifier>doi:10.1007/s11033-024-09520-7</dc:identifier>
  702.    </item>
  703.    <item>
  704.      <title>The interplay of psychosis and non-compliance with fatal outcome in an adult with MSUD</title>
  705.      <link>https://pubmed.ncbi.nlm.nih.gov/38682838/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  706.      <description>Significant progress has been achieved in enhancing early outcomes for individuals with maple syrup urine disease (MSUD), a rare metabolic disorder that leads to the accumulation of branched-chain amino acids leucine, isoleucine, and valine, where leucine is known as the primary neurotoxic metabolite. Newborn screening is helpful in early diagnosis and implementation of dietary treatment, thus reducing neurological deterioration and complications in young children. However, patients face the...</description>
  707.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Am J Med Genet A. 2024 Apr 29:e63637. doi: 10.1002/ajmg.a.63637. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Significant progress has been achieved in enhancing early outcomes for individuals with maple syrup urine disease (MSUD), a rare metabolic disorder that leads to the accumulation of branched-chain amino acids leucine, isoleucine, and valine, where leucine is known as the primary neurotoxic metabolite. Newborn screening is helpful in early diagnosis and implementation of dietary treatment, thus reducing neurological deterioration and complications in young children. However, patients face the life-long challenge of maintaining metabolic control through adherence to a strict low-leucine diet to avoid long-term consequences of chronic hyperleucinemia, which include cognitive deficits, mood disorders, and movement disorders. This case report exemplifies the complex involvement of MSUD in adult survivors. Despite presenting early in life, the patient thrived until the onset of psychiatric symptoms. The subject of this case is a 25-year-old woman with MSUD, who remained in her usual state of health until presentation to the emergency department (ED) with psychosis and altered mental status. However, due to a lack of medical records and poor communication, there was a delay in considering MSUD as a primary cause of her psychiatric symptoms. Although a genetics consultation was later arranged and efforts were made to decrease plasma leucine to the therapeutic range, these interventions proved inadequate in halting her deterioration in health. Her condition worsened within 72 h, culminating in her untimely death. This case emphasizes the comorbidity of psychiatric involvement in MSUD, which contributes to metabolic decompensation that can lead to cerebral edema and death. This case also highlights the pressing need for enhanced strategies for the acute management and long-term care of MSUD patients with psychiatric involvement, particularly in scenarios where mental disturbance could lead to noncompliance.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38682838/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38682838</a> | DOI:<a href=https://doi.org/10.1002/ajmg.a.63637>10.1002/ajmg.a.63637</a></p></div>]]></content:encoded>
  708.      <guid isPermaLink="false">pubmed:38682838</guid>
  709.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  710.      <dc:creator>Nadia Falah</dc:creator>
  711.      <dc:creator>Surekha Pendyal</dc:creator>
  712.      <dc:creator>Cina Sasannejad</dc:creator>
  713.      <dc:creator>Allison Gibson</dc:creator>
  714.      <dc:creator>Yu Lin Lee</dc:creator>
  715.      <dc:creator>Marie McDonald</dc:creator>
  716.      <dc:creator>Dwight Koeberl</dc:creator>
  717.      <dc:date>2024-04-29</dc:date>
  718.      <dc:source>American journal of medical genetics. Part A</dc:source>
  719.      <dc:title>The interplay of psychosis and non-compliance with fatal outcome in an adult with MSUD</dc:title>
  720.      <dc:identifier>pmid:38682838</dc:identifier>
  721.      <dc:identifier>doi:10.1002/ajmg.a.63637</dc:identifier>
  722.    </item>
  723.    <item>
  724.      <title>Effects of Unilateral High Frequency Stimulation of the Subthalamic Nucleus on Risk-avoidant Behavior in a Partial 6-hydroxydopamine Model of Parkinson's Disease</title>
  725.      <link>https://pubmed.ncbi.nlm.nih.gov/38682230/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  726.      <description>CONCLUSIONS: These results suggest that unilateral stimulation of the STN may have minimal effects on risk-avoidant behaviors in PD. However, additional research is required to fully understand the mechanisms responsible for changes in anxiety during STN DBS for PD.</description>
  727.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Integr Neurosci. 2024 Apr 19;23(4):84. doi: 10.31083/j.jin2304084.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a well-established treatment for the motor symptoms of Parkinson's disease (PD). While PD is primarily characterized by motor symptoms such as tremor, rigidity, and bradykinesia, it also involves a range of non-motor symptoms, and anxiety is one of the most common. The relationship between PD and anxiety is complex and can be a result of both pathological neural changes and the psychological and emotional impacts of living with a chronic progressive condition. Managing anxiety in PD is critical for improving the patients' quality of life. However, patients undergoing STN DBS can occasionally experience increased anxiety.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: This study investigates changes in risk-avoidant behavior following STN DBS in a pre-motor animal model of PD under chronic and acute unilateral high frequency stimulation.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: No significant changes in risk-avoidant behaviors were observed in rats who underwent STN DBS compared with sham stimulation controls. Chronic stimulation prevented sensitization in the elevated zero maze.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: These results suggest that unilateral stimulation of the STN may have minimal effects on risk-avoidant behaviors in PD. However, additional research is required to fully understand the mechanisms responsible for changes in anxiety during STN DBS for PD.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38682230/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38682230</a> | DOI:<a href=https://doi.org/10.31083/j.jin2304084>10.31083/j.jin2304084</a></p></div>]]></content:encoded>
  728.      <guid isPermaLink="false">pubmed:38682230</guid>
  729.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  730.      <dc:creator>Sydney G Hillan</dc:creator>
  731.      <dc:creator>Anders J Asp</dc:creator>
  732.      <dc:creator>Leena B Pramanik</dc:creator>
  733.      <dc:creator>Aarushi A Mukerjee</dc:creator>
  734.      <dc:creator>Carter B Mulder</dc:creator>
  735.      <dc:creator>Wendy D Lujan</dc:creator>
  736.      <dc:creator>Jodi L Silvernail</dc:creator>
  737.      <dc:creator>Su-Youne Chang</dc:creator>
  738.      <dc:creator>Suelen L Boschen</dc:creator>
  739.      <dc:creator>J Luis Lujan</dc:creator>
  740.      <dc:date>2024-04-29</dc:date>
  741.      <dc:source>Journal of integrative neuroscience</dc:source>
  742.      <dc:title>Effects of Unilateral High Frequency Stimulation of the Subthalamic Nucleus on Risk-avoidant Behavior in a Partial 6-hydroxydopamine Model of Parkinson's Disease</dc:title>
  743.      <dc:identifier>pmid:38682230</dc:identifier>
  744.      <dc:identifier>doi:10.31083/j.jin2304084</dc:identifier>
  745.    </item>
  746.    <item>
  747.      <title>Causal Relationship between Sex Hormones and Risk of Developing Common Neurodegenerative Diseases: A Mendelian Randomization Study</title>
  748.      <link>https://pubmed.ncbi.nlm.nih.gov/38682222/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  749.      <description>CONCLUSIONS: Elevated BT is associated with a reduced risk of developing ALS. Further research is needed to investigate the underlying mechanisms of action for this correlation and how it can be used as a potential target of action to reduce the risk of developing ALS.</description>
  750.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Integr Neurosci. 2024 Apr 12;23(4):78. doi: 10.31083/j.jin2304078.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Neurodegenerative diseases are a group of unexplained disorders of the central nervous system, and studies have shown that a large number of genetic and environmental factors are associated with these diseases. Since these diseases show significant gender differences in epidemiology, sex hormones are thought to be strongly associated with these diseases. In this study, we used Mendelian randomization to explore the causal relationship between sex hormones and the risk of developing neurodegenerative diseases.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We obtained genetic instrumental variables for sex hormones (sex hormone-binding globulin [SHBG], estradiol levels [EL], and bioavailable testosterone [BT]) separately through the Integrative Epidemiology Unit (IEU) database (https://gwas.mrcieu.ac.uk/). We analyzed the causal relationship of each with the risk of developing neurodegenerative diseases (Amyotrophic Lateral Sclerosis [ALS], Parkinson's disease [PD], and Alzheimer's disease [AD]) using inverse variance weighted (IVW) in Mendelian randomization. Data were then analyzed for sensitivity.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: BT was negatively associated with the risk of developing ALS (odds ratio [OR] = 0.794; 95% confidence interval [95% CI] = 0.672-0.938; <i>p</i> = 0.006). EL and SHBG were not associated with a risk for developing neurodegenerative diseases (ALS, PD, AD).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Elevated BT is associated with a reduced risk of developing ALS. Further research is needed to investigate the underlying mechanisms of action for this correlation and how it can be used as a potential target of action to reduce the risk of developing ALS.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38682222/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38682222</a> | DOI:<a href=https://doi.org/10.31083/j.jin2304078>10.31083/j.jin2304078</a></p></div>]]></content:encoded>
  751.      <guid isPermaLink="false">pubmed:38682222</guid>
  752.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  753.      <dc:creator>Qiang Huang</dc:creator>
  754.      <dc:creator>Qiong Li</dc:creator>
  755.      <dc:creator>Jun-Hong Guo</dc:creator>
  756.      <dc:date>2024-04-29</dc:date>
  757.      <dc:source>Journal of integrative neuroscience</dc:source>
  758.      <dc:title>Causal Relationship between Sex Hormones and Risk of Developing Common Neurodegenerative Diseases: A Mendelian Randomization Study</dc:title>
  759.      <dc:identifier>pmid:38682222</dc:identifier>
  760.      <dc:identifier>doi:10.31083/j.jin2304078</dc:identifier>
  761.    </item>
  762.    <item>
  763.      <title>Clearing the Fog: A Review of Antipsychotics for Parkinson's-Related Hallucinations: A Focus on Pimavanserin, Quetiapine and Clozapine</title>
  764.      <link>https://pubmed.ncbi.nlm.nih.gov/38682215/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  765.      <description>Parkinson's disease is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, including hallucinations. The use of antipsychotic medications is a common strategy to manage hallucinations associated with Parkinson's disease psychosis (PDP). However, careful consideration is necessary when selecting the most appropriate drug due to the potential risks associated with the available treatment options. Atypical antipsychotics (AAPs), such as Pimavanserin and...</description>
  766.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Integr Neurosci. 2024 Apr 12;23(4):80. doi: 10.31083/j.jin2304080.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Parkinson's disease is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, including hallucinations. The use of antipsychotic medications is a common strategy to manage hallucinations associated with Parkinson's disease psychosis (PDP). However, careful consideration is necessary when selecting the most appropriate drug due to the potential risks associated with the available treatment options. Atypical antipsychotics (AAPs), such as Pimavanserin and Clozapine, have effectively controlled PDP symptoms. On the contrary, the support for utilizing quetiapine is not as substantial as other antipsychotics because research studies specifically investigating its application are still emerging and relatively recent. The broad mechanisms of action of AAPs, involving dopamine and serotonin receptors, provide improved outcomes and fewer side effects than typical antipsychotics. Conversely, other antipsychotics, including risperidone, olanzapine, aripiprazole, ziprasidone, and lurasidone, have been found to worsen motor symptoms and are generally not recommended for PDP. While AAPs offer favorable benefits, they are associated with specific adverse effects. Extrapyramidal symptoms, somnolence, hypotension, constipation, and cognitive impairment are commonly observed with AAP use. Clozapine, in particular, carries a risk of agranulocytosis, necessitating close monitoring of blood counts. Pimavanserin, a selective serotonin inverse agonist, avoids receptor-related side effects but has been linked to corrected QT (QTc) interval prolongation, while quetiapine has been reported to be associated with an increased risk of mortality. This review aims to analyze the benefits, risks, and mechanisms of action of antipsychotic medications to assist clinicians in making informed decisions and enhance patient care.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38682215/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38682215</a> | DOI:<a href=https://doi.org/10.31083/j.jin2304080>10.31083/j.jin2304080</a></p></div>]]></content:encoded>
  767.      <guid isPermaLink="false">pubmed:38682215</guid>
  768.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  769.      <dc:creator>Toufik Abdul-Rahman</dc:creator>
  770.      <dc:creator>Ranferi Eduardo Herrera-Calderón</dc:creator>
  771.      <dc:creator>Nicholas Aderinto</dc:creator>
  772.      <dc:creator>Mrinmoy Kundu</dc:creator>
  773.      <dc:creator>Andrew Awuah Wireko</dc:creator>
  774.      <dc:creator>Favour Tope Adebusoye</dc:creator>
  775.      <dc:creator>Olabode Ekerin</dc:creator>
  776.      <dc:creator>Lukman Lawal</dc:creator>
  777.      <dc:creator>Nikitina Iryna Mykolaivna</dc:creator>
  778.      <dc:creator>Athanasios Alexiou</dc:creator>
  779.      <dc:creator>Majed N Almashjary</dc:creator>
  780.      <dc:creator>Asma Perveen</dc:creator>
  781.      <dc:creator>Ghulam Md Ashraf</dc:creator>
  782.      <dc:date>2024-04-29</dc:date>
  783.      <dc:source>Journal of integrative neuroscience</dc:source>
  784.      <dc:title>Clearing the Fog: A Review of Antipsychotics for Parkinson's-Related Hallucinations: A Focus on Pimavanserin, Quetiapine and Clozapine</dc:title>
  785.      <dc:identifier>pmid:38682215</dc:identifier>
  786.      <dc:identifier>doi:10.31083/j.jin2304080</dc:identifier>
  787.    </item>
  788.    <item>
  789.      <title>Electrocardiographic approach strategies in patients with Parkinson disease treated with deep brain stimulation</title>
  790.      <link>https://pubmed.ncbi.nlm.nih.gov/38682099/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  791.      <description>Deep brain stimulation (DBS) is an interdisciplinary and reversible therapy that uses high-frequency electrical stimulation to correct aberrant neural pathways in motor and cognitive neurological disorders. However, the high frequency of the waves used in DBS can interfere with electrical recording devices (e.g., electrocardiogram, electroencephalogram, cardiac monitor), creating artifacts that hinder their interpretation. The compatibility of DBS with these devices varies and depends on factors...</description>
  792.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Front Cardiovasc Med. 2024 Apr 12;11:1265089. doi: 10.3389/fcvm.2024.1265089. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Deep brain stimulation (DBS) is an interdisciplinary and reversible therapy that uses high-frequency electrical stimulation to correct aberrant neural pathways in motor and cognitive neurological disorders. However, the high frequency of the waves used in DBS can interfere with electrical recording devices (e.g., electrocardiogram, electroencephalogram, cardiac monitor), creating artifacts that hinder their interpretation. The compatibility of DBS with these devices varies and depends on factors such as the underlying disease and the configuration of the neurostimulator. In emergencies where obtaining an electrocardiogram is crucial, the need for more consensus on reducing electrical artifacts in patients with DBS becomes a significant challenge. Various strategies have been proposed to attenuate the artifact generated by DBS, such as changing the DBS configuration from monopolar to bipolar, temporarily deactivating DBS during electrocardiographic recording, applying frequency filters both lower and higher than those used by DBS, and using non-standard leads. However, the inexperience of medical personnel, variability in DBS models, or the lack of a controller at the time of approach limit the application of these strategies. Current evidence on their reproducibility and efficacy is limited. Due to the growing elderly population and the rising utilization of DBS, it is imperative to create electrocardiographic methods that are easily accessible and reproducible for general physicians and emergency services.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38682099/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38682099</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11047133/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11047133</a> | DOI:<a href=https://doi.org/10.3389/fcvm.2024.1265089>10.3389/fcvm.2024.1265089</a></p></div>]]></content:encoded>
  793.      <guid isPermaLink="false">pubmed:38682099</guid>
  794.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  795.      <dc:creator>Carlos Rafael Sierra-Fernández</dc:creator>
  796.      <dc:creator>Luis Rodrigo Garnica-Geronimo</dc:creator>
  797.      <dc:creator>Alejandra Huipe-Dimas</dc:creator>
  798.      <dc:creator>Jorge A Ortega-Hernandez</dc:creator>
  799.      <dc:creator>María Alejandra Ruiz-Mafud</dc:creator>
  800.      <dc:creator>Amin Cervantes-Arriaga</dc:creator>
  801.      <dc:creator>Ana Jimena Hernández-Medrano</dc:creator>
  802.      <dc:creator>Mayela Rodríguez-Violante</dc:creator>
  803.      <dc:date>2024-04-29</dc:date>
  804.      <dc:source>Frontiers in cardiovascular medicine</dc:source>
  805.      <dc:title>Electrocardiographic approach strategies in patients with Parkinson disease treated with deep brain stimulation</dc:title>
  806.      <dc:identifier>pmid:38682099</dc:identifier>
  807.      <dc:identifier>pmc:PMC11047133</dc:identifier>
  808.      <dc:identifier>doi:10.3389/fcvm.2024.1265089</dc:identifier>
  809.    </item>
  810.    <item>
  811.      <title>Chronically socially isolated mice exhibit depressive-like behavior regulated by the gut microbiota</title>
  812.      <link>https://pubmed.ncbi.nlm.nih.gov/38681644/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  813.      <description>CONCLUSION: CSI induces a dysbiotic gut microbiota and the production of neurorelated metabolites, which in turn increase inflammatory responses and result in depressive behaviors in CSI mice. Therefore, these findings suggest that the gut microbiota may serve as a target for the treatment of long-term social isolation-induced mental disorders.</description>
  814.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Heliyon. 2024 Apr 18;10(8):e29791. doi: 10.1016/j.heliyon.2024.e29791. eCollection 2024 Apr 30.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: Chronic loneliness is a widespread issue, and the gut-brain axis is known to be crucial in facilitating communication between the gut and brain. However, the precise mechanism by which chronic loneliness affects the gut-brain axis remains uncertain.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Fourteen 55-week-old Balb/c mice were used in the experiment, with seven mice being randomly assigned to the chronic social isolation (CSI) group. The CSI group mice underwent 12 weeks of isolation to simulate the psychiatric state of a population in prolonged social isolation. The mental state of the CSI mice was assessed through animal behavior analysis, while plasma cytokines were measured using ELISA. Additionally, the composition of the gut microbiota was analyzed using 16S rRNA sequencing, and the metabolite composition of the intestinal contents was examined using nontargeted metabolomics. The Student-T test was used to determine significant mean differences.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Mice that were exposed to the CSI exhibited increased immobility time lengths in forced swimming and hanging tail experiments, and decreased movement lengths and number of times traversing the intermediate region, compared to control mice. Additionally, CSI decreased the abundance of the probiotics Ruminococcaceae, Akkermansiaceae, and Christensenellaceae. Additionally, CSI reduced the production of the metabolites oleamide and tryptophan. Furthermore, IL-1β, IL-4, and IL-6 were significantly increased, while TNF-α was significantly decreased.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSION: CSI induces a dysbiotic gut microbiota and the production of neurorelated metabolites, which in turn increase inflammatory responses and result in depressive behaviors in CSI mice. Therefore, these findings suggest that the gut microbiota may serve as a target for the treatment of long-term social isolation-induced mental disorders.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38681644/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38681644</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11046198/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11046198</a> | DOI:<a href=https://doi.org/10.1016/j.heliyon.2024.e29791>10.1016/j.heliyon.2024.e29791</a></p></div>]]></content:encoded>
  815.      <guid isPermaLink="false">pubmed:38681644</guid>
  816.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  817.      <dc:creator>Linwei Ding</dc:creator>
  818.      <dc:creator>Jiaqi Liu</dc:creator>
  819.      <dc:creator>Yunjia Yang</dc:creator>
  820.      <dc:creator>Zeying Cui</dc:creator>
  821.      <dc:creator>Guankui Du</dc:creator>
  822.      <dc:date>2024-04-29</dc:date>
  823.      <dc:source>Heliyon</dc:source>
  824.      <dc:title>Chronically socially isolated mice exhibit depressive-like behavior regulated by the gut microbiota</dc:title>
  825.      <dc:identifier>pmid:38681644</dc:identifier>
  826.      <dc:identifier>pmc:PMC11046198</dc:identifier>
  827.      <dc:identifier>doi:10.1016/j.heliyon.2024.e29791</dc:identifier>
  828.    </item>
  829.    <item>
  830.      <title>A Role for GABA&lt;sub&gt;A&lt;/sub&gt; Receptor β3 Subunits in Mediating Harmaline Tremor Suppression by Alcohol: Implications for Essential Tremor Therapy</title>
  831.      <link>https://pubmed.ncbi.nlm.nih.gov/38681506/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  832.      <description>BACKGROUND: Essential tremor patients may find that low alcohol amounts suppress tremor. A candidate mechanism is modulation of α6β3δ extra-synaptic GABA(A) receptors, that in vitro respond to non-intoxicating alcohol levels. We previously found that low-dose alcohol reduces harmaline tremor in wild-type mice, but not in littermates lacking δ or α6 subunits. Here we addressed whether low-dose alcohol requires the β3 subunit for tremor suppression.</description>
  833.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Tremor Other Hyperkinet Mov (N Y). 2024 Apr 26;14:20. doi: 10.5334/tohm.834. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Essential tremor patients may find that low alcohol amounts suppress tremor. A candidate mechanism is modulation of α6β3δ extra-synaptic GABA<sub>A</sub> receptors, that <i>in vitro</i> respond to non-intoxicating alcohol levels. We previously found that low-dose alcohol reduces harmaline tremor in wild-type mice, but not in littermates lacking δ or α6 subunits. Here we addressed whether low-dose alcohol requires the β3 subunit for tremor suppression.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We tested whether low-dose alcohol suppresses tremor in cre-negative mice with intact β3 exon 3 flanked by loxP, and in littermates in which this region was excised by cre expressed under the α6 subunit promotor. Tremor in the harmaline model was measured as a percentage of motion power in the tremor bandwidth divided by overall motion power.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Alcohol, 0.500 and 0.575 g/kg, reduced harmaline tremor compared to vehicle-treated controls in floxed β3 cre- mice, but had no effect on tremor in floxed β3 cre+ littermates that have β3 knocked out. This was not due to potential interference of α6 expression by the insertion of the cre gene into the α6 gene since non-floxed β3 cre+ and cre- littermates exhibited similar tremor suppression by alcohol.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">DISCUSSION: As α6β3δ GABA<sub>A</sub> receptors are sensitive to low-dose alcohol, and cerebellar granule cells express β3 and are the predominant brain site for α6 and δ expression together, our overall findings suggest alcohol acts to suppress tremor by modulating α6β3δ GABA<sub>A</sub> receptors on these cells. Novel drugs that target this receptor may potentially be effective and well-tolerated for essential tremor.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">HIGHLIGHTS: We previously found with the harmaline essential tremor model that GABA<sub>A</sub> receptors containing α6 and δ subunits mediate tremor suppression by alcohol. We now show that β3 subunits in α6-expressing cells, likely cerebellar granule cells, are also required, indicating that alcohol suppresses tremor by modulating α6β3δ extra-synaptic GABA<sub>A</sub> receptors.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38681506/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38681506</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11049614/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11049614</a> | DOI:<a href=https://doi.org/10.5334/tohm.834>10.5334/tohm.834</a></p></div>]]></content:encoded>
  834.      <guid isPermaLink="false">pubmed:38681506</guid>
  835.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  836.      <dc:creator>Adrian Handforth</dc:creator>
  837.      <dc:creator>Ram P Singh</dc:creator>
  838.      <dc:creator>Hovsep P Kosoyan</dc:creator>
  839.      <dc:creator>Pournima A Kadam</dc:creator>
  840.      <dc:date>2024-04-29</dc:date>
  841.      <dc:source>Tremor and other hyperkinetic movements (New York, N.Y.)</dc:source>
  842.      <dc:title>A Role for GABA&lt;sub&gt;A&lt;/sub&gt; Receptor β3 Subunits in Mediating Harmaline Tremor Suppression by Alcohol: Implications for Essential Tremor Therapy</dc:title>
  843.      <dc:identifier>pmid:38681506</dc:identifier>
  844.      <dc:identifier>pmc:PMC11049614</dc:identifier>
  845.      <dc:identifier>doi:10.5334/tohm.834</dc:identifier>
  846.    </item>
  847.    <item>
  848.      <title>Posterior Interosseous Neuropathy with Peripheral Dystonia: A Case Report</title>
  849.      <link>https://pubmed.ncbi.nlm.nih.gov/38681505/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  850.      <description>BACKGROUND: Posterior interosseous neuropathy is an uncommon cause of peripheral dystonia.</description>
  851.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Tremor Other Hyperkinet Mov (N Y). 2024 Apr 22;14:19. doi: 10.5334/tohm.856. eCollection 2024.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Posterior interosseous neuropathy is an uncommon cause of peripheral dystonia.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CASE REPORT: A 62-year-old man awakened and noticed right finger drop. A neurological examination revealed posterior interosseous neuropathy with dystonia-like finger movements. Abnormal movements were predominantly observed in the right thumb, ring finger, and little finger. Within 2 weeks, the muscle weakness in the right fingers had completely improved. However, a brief abnormal posture of the right thumb was persistent.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">DISCUSSION: The residual abnormal posture of the right thumb may reflect pre-existing motor control abnormalities, which may have contributed to the onset of posterior interosseous neuropathy-associated peripheral dystonia.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38681505/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38681505</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11049617/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11049617</a> | DOI:<a href=https://doi.org/10.5334/tohm.856>10.5334/tohm.856</a></p></div>]]></content:encoded>
  852.      <guid isPermaLink="false">pubmed:38681505</guid>
  853.      <pubDate>Mon, 29 Apr 2024 06:00:00 -0400</pubDate>
  854.      <dc:creator>Gohei Yamada</dc:creator>
  855.      <dc:creator>Takanari Toyoda</dc:creator>
  856.      <dc:creator>Eiichi Katada</dc:creator>
  857.      <dc:creator>Noriyuki Matsukawa</dc:creator>
  858.      <dc:date>2024-04-29</dc:date>
  859.      <dc:source>Tremor and other hyperkinetic movements (New York, N.Y.)</dc:source>
  860.      <dc:title>Posterior Interosseous Neuropathy with Peripheral Dystonia: A Case Report</dc:title>
  861.      <dc:identifier>pmid:38681505</dc:identifier>
  862.      <dc:identifier>pmc:PMC11049617</dc:identifier>
  863.      <dc:identifier>doi:10.5334/tohm.856</dc:identifier>
  864.    </item>
  865.    <item>
  866.      <title>Nervonic acid alleviates MPTP-induced Parkinson's disease via MEK/ERK pathway</title>
  867.      <link>https://pubmed.ncbi.nlm.nih.gov/38678620/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  868.      <description>Nervonic acid (NA) is a primary long-chain fatty acid and has been confirmed to have neuroprotective effects in neurologic diseases. Oxidative stress and neuronal damage are the main causes of Parkinson's disease (PD). This study mainly explored whether NA is involved in regulating oxidative stress and apoptosis in MPTP-induced mouse model and MPP-induced cell model. Through behavior tests, we proved that MPTP-induced motor dysfunction in mice was recovered by NA treatment. NA can reduce...</description>
  869.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Mol Biol (Noisy-le-grand). 2024 Apr 28;70(4):100-106. doi: 10.14715/cmb/2024.70.4.16.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Nervonic acid (NA) is a primary long-chain fatty acid and has been confirmed to have neuroprotective effects in neurologic diseases. Oxidative stress and neuronal damage are the main causes of Parkinson's disease (PD). This study mainly explored whether NA is involved in regulating oxidative stress and apoptosis in MPTP-induced mouse model and MPP-induced cell model. Through behavior tests, we proved that MPTP-induced motor dysfunction in mice was recovered by NA treatment. NA can reduce MPTP-induced neuronal damage, manifested by elevated levels of TH and dopamine, as well as decreased levels of α-syn. In the in vitro model, we observed from CCK8 assay and flow cytometry that the induction of MPP markedly suppressed cell activity and enhanced cell apoptosis, but these functions were all reversed by NA. Furthermore, NA administration reversed the increase in ROS production and MDA levels induced by MPTP or MPP, as well as the decrease in SOD levels, suggesting the antioxidant properties of NA in PD. Meanwhile, we confirmed that NA can regulate oxidative stress and neuronal damage by activating the MEK/ERK pathway. Overall, we concluded that NA could alleviate MPTP-induced PD via MEK/ERK pathway.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38678620/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38678620</a> | DOI:<a href=https://doi.org/10.14715/cmb/2024.70.4.16>10.14715/cmb/2024.70.4.16</a></p></div>]]></content:encoded>
  870.      <guid isPermaLink="false">pubmed:38678620</guid>
  871.      <pubDate>Sun, 28 Apr 2024 06:00:00 -0400</pubDate>
  872.      <dc:creator>Xinru Zhang</dc:creator>
  873.      <dc:creator>Donglei Wu</dc:creator>
  874.      <dc:creator>Zengwei Yin</dc:creator>
  875.      <dc:date>2024-04-28</dc:date>
  876.      <dc:source>Cellular and molecular biology (Noisy-le-Grand, France)</dc:source>
  877.      <dc:title>Nervonic acid alleviates MPTP-induced Parkinson's disease via MEK/ERK pathway</dc:title>
  878.      <dc:identifier>pmid:38678620</dc:identifier>
  879.      <dc:identifier>doi:10.14715/cmb/2024.70.4.16</dc:identifier>
  880.    </item>
  881.    <item>
  882.      <title>Omega-3 polyunsaturated fatty acids play a protective role in a mouse model of Parkinson's disease by increasing intestinal inducible Treg cells</title>
  883.      <link>https://pubmed.ncbi.nlm.nih.gov/38678615/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  884.      <description>Parkinson's disease (PD) is defined as a progressive neurodegenerative disease in middle-aged and elderly people. The therapeutic effect of ω-3 PUFAs in several neurodegenerative diseases has been well recognized. Nevertheless, whether nutrition supplementing ω-3 PUFAs exerts a neuroprotective role in PD remains elusive. Bioinformatics revealed 2D chemical structural formula of three components. Mice received indicated treatment with saline, MPTP or ω-3 PUFAs according to grouping. Behavioral...</description>
  885.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Cell Mol Biol (Noisy-le-grand). 2024 Apr 28;70(4):107-112. doi: 10.14715/cmb/2024.70.4.17.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Parkinson's disease (PD) is defined as a progressive neurodegenerative disease in middle-aged and elderly people. The therapeutic effect of ω-3 PUFAs in several neurodegenerative diseases has been well recognized. Nevertheless, whether nutrition supplementing ω-3 PUFAs exerts a neuroprotective role in PD remains elusive. Bioinformatics revealed 2D chemical structural formula of three components. Mice received indicated treatment with saline, MPTP or ω-3 PUFAs according to grouping. Behavioral function of mice was measured through motor tests such as rearing, akinesia, and rotarod tests. OFT test measured anxiety-like behaviors of mice. Western blotting and TUNEL staining measured dopaminergic fibers and neurons of mice. Western blotting measured inflammation and apoptosis-related protein levels in mouse tissue. FACS measured iTreg cell proportion in colon and brain tissues of mice. ω-3 PUFAs repaired MPTP-stimulated motor function damage in PD mice. ω-3 PUFAs mitigated MPTP-stimulated comorbid anxiety in PD mice. ω-3 PUFAs relieved MPTP-stimulated deficits of dopaminergic fibers and neurons in PD mice. ω-3 PUFAs repressed MPTP-stimulated inflammation and apoptosis pathway activation in PD mice. ω-3 PUFAs repaired MPTP-stimulated immune function damage in PD mice. ω-3 PUFAs exert a protective role in PD mice through alleviating motor function impairment and neuroinflammation by increasing intestinal inducible Treg cells, which may provide a new direction for seeking targeted therapy plans for PD in humans.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38678615/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38678615</a> | DOI:<a href=https://doi.org/10.14715/cmb/2024.70.4.17>10.14715/cmb/2024.70.4.17</a></p></div>]]></content:encoded>
  886.      <guid isPermaLink="false">pubmed:38678615</guid>
  887.      <pubDate>Sun, 28 Apr 2024 06:00:00 -0400</pubDate>
  888.      <dc:creator>Yezi Xia</dc:creator>
  889.      <dc:creator>Yinwei Zhang</dc:creator>
  890.      <dc:creator>Ying Li</dc:creator>
  891.      <dc:creator>Xiaojing Li</dc:creator>
  892.      <dc:creator>Yaling Wu</dc:creator>
  893.      <dc:creator>Qi Yao</dc:creator>
  894.      <dc:date>2024-04-28</dc:date>
  895.      <dc:source>Cellular and molecular biology (Noisy-le-Grand, France)</dc:source>
  896.      <dc:title>Omega-3 polyunsaturated fatty acids play a protective role in a mouse model of Parkinson's disease by increasing intestinal inducible Treg cells</dc:title>
  897.      <dc:identifier>pmid:38678615</dc:identifier>
  898.      <dc:identifier>doi:10.14715/cmb/2024.70.4.17</dc:identifier>
  899.    </item>
  900.    <item>
  901.      <title>Effects of Inpatient Occupational Rehabilitation vs. Outpatient Acceptance and Commitment Therapy on Sick Leave and Cost of Lost Production: 7-Year Follow-Up of a Randomized Controlled Trial</title>
  902.      <link>https://pubmed.ncbi.nlm.nih.gov/38678497/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  903.      <description>CONCLUSIONS: I-MORE outperformed O-ACT in reducing sickness absence and production loss costs during seven years of follow-up, but due to a limited sample size the results were unprecise. Considering the potential for substantial societal cost savings from reduced sick leave, there is a need for larger, long-term studies to evaluate return-to-work interventions.</description>
  904.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Occup Rehabil. 2024 Apr 28. doi: 10.1007/s10926-024-10195-x. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">OBJECTIVES: Previously, we reported that an inpatient multimodal occupational rehabilitation program (I-MORE) was more effective than outpatient Acceptance and Commitment Therapy (O-ACT) in reducing sickness absence and was cost-effective over a 24-month period. Here we present 7-years of follow-up on sick leave and the cost of lost production.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We randomized individuals aged 18-60, sick-listed due to musculoskeletal or mental health disorders to I-MORE (n = 82) or O-ACT (n = 79). I-MORE, lasting 3.5 weeks, integrated ACT, physical training, and work-related problem-solving. In contrast, O-ACT mainly offered six weekly 2.5 h group sessions of ACT. We measured outcomes using registry data for days on medical benefits and calculated costs of lost production. Our analysis included regression analyses to examine differences in sickness absence days, logistic general estimating equations for repeated events, and generalized linear models to assess differences in costs of lost production.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Unadjusted regression analyses showed 80 fewer days of sickness absence in the 7-year follow-up for I-MORE compared to O-ACT (95% CI - 264 to 104), with an adjusted difference of 114 fewer days (95% CI - 298 to 71). The difference in costs of production loss in favour of I-MORE was 27,048 euros per participant (95% CI - 35,009 to 89,104).</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: I-MORE outperformed O-ACT in reducing sickness absence and production loss costs during seven years of follow-up, but due to a limited sample size the results were unprecise. Considering the potential for substantial societal cost savings from reduced sick leave, there is a need for larger, long-term studies to evaluate return-to-work interventions.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38678497/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38678497</a> | DOI:<a href=https://doi.org/10.1007/s10926-024-10195-x>10.1007/s10926-024-10195-x</a></p></div>]]></content:encoded>
  905.      <guid isPermaLink="false">pubmed:38678497</guid>
  906.      <pubDate>Sun, 28 Apr 2024 06:00:00 -0400</pubDate>
  907.      <dc:creator>Lene Aasdahl</dc:creator>
  908.      <dc:creator>Sigmund Østgård Gismervik</dc:creator>
  909.      <dc:creator>Roar Johnsen</dc:creator>
  910.      <dc:creator>Ottar Vasseljen</dc:creator>
  911.      <dc:creator>Gudrun M W Bjørnelv</dc:creator>
  912.      <dc:creator>Johan Håkon Bjørngaard</dc:creator>
  913.      <dc:creator>Marius Steiro Fimland</dc:creator>
  914.      <dc:date>2024-04-28</dc:date>
  915.      <dc:source>Journal of occupational rehabilitation</dc:source>
  916.      <dc:title>Effects of Inpatient Occupational Rehabilitation vs. Outpatient Acceptance and Commitment Therapy on Sick Leave and Cost of Lost Production: 7-Year Follow-Up of a Randomized Controlled Trial</dc:title>
  917.      <dc:identifier>pmid:38678497</dc:identifier>
  918.      <dc:identifier>doi:10.1007/s10926-024-10195-x</dc:identifier>
  919.    </item>
  920.    <item>
  921.      <title>Vertical locomotion improves horizontal locomotion: effects of climbing on gait and other mobility aspects in Parkinson's disease. A secondary analysis from a randomized controlled trial</title>
  922.      <link>https://pubmed.ncbi.nlm.nih.gov/38678241/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  923.      <description>CONCLUSIONS: Sport climbing improves gait speed during normal and fast walking, as well as functional mobility in people with Parkinson's disease. Trial registration This study was registered within the U.S. National Library of Medicine (No: NCT04569981, date of registration September 30th, 2020).</description>
  924.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">J Neuroeng Rehabil. 2024 Apr 27;21(1):63. doi: 10.1186/s12984-024-01363-4.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: In the Climb Up! Head Up! trial, we showed that sport climbing reduces bradykinesia, tremor, and rigidity in mildly to moderately affected participants with Parkinson's disease. This secondary analysis aimed to evaluate the effects of sport climbing on gait and functional mobility in this cohort.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: Climb Up! Head Up! was a 1:1 randomized controlled trial. Forty-eight PD participants (Hoehn and Yahr stage 2-3) either participated in a 12-week, 90-min-per-week sport climbing course (intervention group) or were engaged in regular unsupervised physical activity (control group). Relevant outcome measures for this analysis were extracted from six inertial measurement units placed on the extremities, chest, and lower back, that were worn during supervised gait and functional mobility assessments before and after the intervention. Assessments included normal and fast walking, dual-tasking walking, Timed Up and Go test, Instrumented Stand and Walk test, and Five Times Sit to Stand test.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: Compared to baseline, climbing improved gait speed during normal walking by 0.09 m/s (p = 0.005) and during fast walking by 0.1 m/s. Climbing also reduced the time spent in the stance phase during fast walking by 0.03 s. Climbing improved the walking speed in the 7-m- Timed Up and Go test by 0.1 m/s (p &lt; 0.001) and the turning speed by 0.39 s (p = 0.052), the speed in the Instrumented Stand and Walk test by 0.1 m/s (p &lt; 0.001), and the speed in the Five Times Sit to Stand test by 2.5 s (p = 0.014). There was no effect of sport climbing on gait speed or gait variables during dual-task walking.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Sport climbing improves gait speed during normal and fast walking, as well as functional mobility in people with Parkinson's disease. Trial registration This study was registered within the U.S. National Library of Medicine (No: NCT04569981, date of registration September 30th, 2020).</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38678241/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38678241</a> | PMC:<a href="https://www.ncbi.nlm.nih.gov/pmc/PMC11055236/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">PMC11055236</a> | DOI:<a href=https://doi.org/10.1186/s12984-024-01363-4>10.1186/s12984-024-01363-4</a></p></div>]]></content:encoded>
  925.      <guid isPermaLink="false">pubmed:38678241</guid>
  926.      <pubDate>Sat, 27 Apr 2024 06:00:00 -0400</pubDate>
  927.      <dc:creator>Agnes Langer</dc:creator>
  928.      <dc:creator>Clint Hansen</dc:creator>
  929.      <dc:creator>Dominik Roth</dc:creator>
  930.      <dc:creator>Agnes Santer</dc:creator>
  931.      <dc:creator>Anna Flotz</dc:creator>
  932.      <dc:creator>Jakob Gruber</dc:creator>
  933.      <dc:creator>Laurenz Wizany</dc:creator>
  934.      <dc:creator>Sebastian Hasenauer</dc:creator>
  935.      <dc:creator>Rochus Pokan</dc:creator>
  936.      <dc:creator>Peter Dabnichki</dc:creator>
  937.      <dc:creator>Marco Treven</dc:creator>
  938.      <dc:creator>Sarah Zimmel</dc:creator>
  939.      <dc:creator>Michaela Schmoeger</dc:creator>
  940.      <dc:creator>Ulrike Willinger</dc:creator>
  941.      <dc:creator>Lucia Gassner</dc:creator>
  942.      <dc:creator>Christof Brücke</dc:creator>
  943.      <dc:creator>Walter Maetzler</dc:creator>
  944.      <dc:creator>Heidemarie Zach</dc:creator>
  945.      <dc:date>2024-04-27</dc:date>
  946.      <dc:source>Journal of neuroengineering and rehabilitation</dc:source>
  947.      <dc:title>Vertical locomotion improves horizontal locomotion: effects of climbing on gait and other mobility aspects in Parkinson's disease. A secondary analysis from a randomized controlled trial</dc:title>
  948.      <dc:identifier>pmid:38678241</dc:identifier>
  949.      <dc:identifier>pmc:PMC11055236</dc:identifier>
  950.      <dc:identifier>doi:10.1186/s12984-024-01363-4</dc:identifier>
  951.    </item>
  952.    <item>
  953.      <title>Microglia differential genes and their functions in paraquat-induced Parkinson's disease-like in mice's brains based on single-cell RNA sequencing</title>
  954.      <link>https://pubmed.ncbi.nlm.nih.gov/38677987/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  955.      <description>Objective: To analyze the differential genes and related signaling pathways of microglia subpopulations in Parkinson's disease (PD) -like mouse brains induced by paraquat (PQ) based on single-cell RNA sequencing, and provide clues to elucidate the mechanism of PQ-induced PD-like changes in the brain of animals. Methods: In September 2021, six male 6-week-old C57BL/6 mice were randomly divided into control group and experimental group (three mice in each group) . The mice were injected with...</description>
  956.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2024 Apr 20;42(4):248-257. doi: 10.3760/cma.j.cn121094-20230524-00184.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one"><b>Objective:</b> To analyze the differential genes and related signaling pathways of microglia subpopulations in Parkinson's disease (PD) -like mouse brains induced by paraquat (PQ) based on single-cell RNA sequencing, and provide clues to elucidate the mechanism of PQ-induced PD-like changes in the brain of animals. <b>Methods:</b> In September 2021, six male 6-week-old C57BL/6 mice were randomly divided into control group and experimental group (three mice in each group) . The mice were injected with saline, 10.0 mg/kg PQ intraperitoneally, once every three days, and 10 consecutive injections were used for modeling. After infection, the brains of mice were taken and 10×Genomics single-cell RNA sequencing was performed. Microglia subpopulations were screened based on gene expression characteristics, and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed. The differential genes of microglia subpopulations between the experimental group and control group were further screened, and functional enrichment analysis was performed using bioinformatics tools. Mouse microglia (BV2 cells) were treated with 0, 60, 90 μmol/L PQ solution, respectively. And real-time fluorescence quantitative PCR experiments were conducted to validate the expressions of differential genes hexokinase 2 (Hk2) , ATPase H+ Transporting V0 Subunit B (Atp6v0b) and Neuregulin 1 (Nrg1) . <b>Results:</b> Cluster 7 and Cluster 20 were identified as microglia subpopulations based on the signature genes inositol polyphosphate-5-phosphatase d, Inpp5d (Inpp5d) and transforming growth factor beta receptor 1 (Tgfbr1) , and they reflected the microglia-activated M2 phenotype. The bioinformatics analysis showed that the characteristic genes of identified microglia subpopulations were enriched in endocytosis. In terms of molecular function, it mainly enriched in transmembrane receptor protein kinase activity and cytokine binding. The up-regulated genes of Cluster 7 were mainly enriched in lysosomal pathway, endocytosis pathway, and down-regulated genes were mainly enriched in neurodegenerative disease and other signaling pathways. The up-regulated genes of Cluster 20 were mainly enriched in signaling pathways related to PD, and down-regulated genes were mainly enriched in cyclic adenosine 3', 5'-monophosphate (cAMP) signaling pathways, neurological development, synaptic function and other signaling pathways. The results of real-time fluorescence quantitative PCR showed that the expressions of Hk2 mRNA and Atp6v0b mRNA increased and the expression of Nrg1 mRNA decreased in the 90 μmol/L PQ-treated BV2 cells compared with the 0 μmol/L, and the differences were statistically significant (<i>P</i>&lt;0.05) . <b>Conclusion:</b> Microglia are activated in the PQ-induced PD-like mouse model and polarized toward the M2 phenotype. And their functions are associated with lysosomal (endocytosis) , synaptic functions and the regulation of PD-related pathways.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38677987/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38677987</a> | DOI:<a href=https://doi.org/10.3760/cma.j.cn121094-20230524-00184>10.3760/cma.j.cn121094-20230524-00184</a></p></div>]]></content:encoded>
  957.      <guid isPermaLink="false">pubmed:38677987</guid>
  958.      <pubDate>Sat, 27 Apr 2024 06:00:00 -0400</pubDate>
  959.      <dc:creator>Z K Guo</dc:creator>
  960.      <dc:creator>Y T Zhang</dc:creator>
  961.      <dc:creator>Y Zhang</dc:creator>
  962.      <dc:creator>Y L Weng</dc:creator>
  963.      <dc:creator>H Y Li</dc:creator>
  964.      <dc:creator>S Y Wu</dc:creator>
  965.      <dc:date>2024-04-27</dc:date>
  966.      <dc:source>Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases</dc:source>
  967.      <dc:title>Microglia differential genes and their functions in paraquat-induced Parkinson's disease-like in mice's brains based on single-cell RNA sequencing</dc:title>
  968.      <dc:identifier>pmid:38677987</dc:identifier>
  969.      <dc:identifier>doi:10.3760/cma.j.cn121094-20230524-00184</dc:identifier>
  970.    </item>
  971.    <item>
  972.      <title>Better identifying and understanding post-traumatic stress disorder in the elderly</title>
  973.      <link>https://pubmed.ncbi.nlm.nih.gov/38677805/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  974.      <description>Post-traumatic stress disorder (PTSD) is particularly common in the elderly, including those with cognitive impairments. We need to stress the importance of early detection to better understand the specific signs of this disorder in the elderly. Psychotherapies such as cognitive-behavioral therapy and Eye Movement Desensitization and Reprocessing are being explored for their effectiveness and adaptability with the elderly. Identifying post-traumatic stress disorder should be a shared...</description>
  975.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Soins Gerontol. 2024 May-Jun;29(167):14-18. doi: 10.1016/j.sger.2024.02.004. Epub 2024 Apr 2.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Post-traumatic stress disorder (PTSD) is particularly common in the elderly, including those with cognitive impairments. We need to stress the importance of early detection to better understand the specific signs of this disorder in the elderly. Psychotherapies such as cognitive-behavioral therapy and Eye Movement Desensitization and Reprocessing are being explored for their effectiveness and adaptability with the elderly. Identifying post-traumatic stress disorder should be a shared responsibility, for the mental health of the elderly.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38677805/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38677805</a> | DOI:<a href=https://doi.org/10.1016/j.sger.2024.02.004>10.1016/j.sger.2024.02.004</a></p></div>]]></content:encoded>
  976.      <guid isPermaLink="false">pubmed:38677805</guid>
  977.      <pubDate>Sat, 27 Apr 2024 06:00:00 -0400</pubDate>
  978.      <dc:creator>Jean Roche</dc:creator>
  979.      <dc:creator>Anne-Julie Vaillant-Ciszewicz</dc:creator>
  980.      <dc:creator>Olivier Guerin</dc:creator>
  981.      <dc:date>2024-04-27</dc:date>
  982.      <dc:source>Soins. Gerontologie</dc:source>
  983.      <dc:title>Better identifying and understanding post-traumatic stress disorder in the elderly</dc:title>
  984.      <dc:identifier>pmid:38677805</dc:identifier>
  985.      <dc:identifier>doi:10.1016/j.sger.2024.02.004</dc:identifier>
  986.    </item>
  987.    <item>
  988.      <title>Effects of atrazine on movement, metabolism and gene expression in Pelophylax nigromaculatus larvae under global warming</title>
  989.      <link>https://pubmed.ncbi.nlm.nih.gov/38677404/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  990.      <description>Global warming and environmental pollutants both pose a threat to the behavior and physiology of animals, but research on the combined effects of the two is limited. Atrazine, a widely used herbicide, has toxic effects on organisms. In this study, the effects of environmental concentrations of atrazine exposure (100 μg/L ) for seven days on the movement, metabolism and gene expression related to motility of Pelophylax nigromaculatus larvae (GS8) were investigated under global warming. The...</description>
  991.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Environ Res. 2024 Apr 25:119007. doi: 10.1016/j.envres.2024.119007. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">Global warming and environmental pollutants both pose a threat to the behavior and physiology of animals, but research on the combined effects of the two is limited. Atrazine, a widely used herbicide, has toxic effects on organisms. In this study, the effects of environmental concentrations of atrazine exposure (100 μg/L ) for seven days on the movement, metabolism and gene expression related to motility of Pelophylax nigromaculatus larvae (GS8) were investigated under global warming. The results showed that compared to the optimal growth temperature (18°C), atrazine treatment under global warming (21°C) significantly increased the average speed (about 11.2 times) and maximum acceleration (about 1.98 times) of P. nigromaculatus larvae, altered the relative abundance of 539 metabolites, including Formyl-5-hydroxykynurenamine, 2,4-Dihydroxybenzophenone, and FAPy-adenine, and changed the nucleotide metabolism, pyrimidine metabolism, glycerophospholipid metabolism, and purine metabolism, as well as increased the gene expression of SPLA2 (about 6.46 times) and CHK (about 3.25 times). In summary, atrazine treatment under global warming caused metabolic disorders in amphibian larvae and increased the expression of some movement-related genes in the brain, resulting in abnormally active.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38677404/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38677404</a> | DOI:<a href=https://doi.org/10.1016/j.envres.2024.119007>10.1016/j.envres.2024.119007</a></p></div>]]></content:encoded>
  992.      <guid isPermaLink="false">pubmed:38677404</guid>
  993.      <pubDate>Sat, 27 Apr 2024 06:00:00 -0400</pubDate>
  994.      <dc:creator>Jiawei Yin</dc:creator>
  995.      <dc:creator>Minyi Huang</dc:creator>
  996.      <dc:creator>Renyan Duan</dc:creator>
  997.      <dc:creator>Wentao Huang</dc:creator>
  998.      <dc:creator>Yuhao Zhang</dc:creator>
  999.      <dc:date>2024-04-27</dc:date>
  1000.      <dc:source>Environmental research</dc:source>
  1001.      <dc:title>Effects of atrazine on movement, metabolism and gene expression in Pelophylax nigromaculatus larvae under global warming</dc:title>
  1002.      <dc:identifier>pmid:38677404</dc:identifier>
  1003.      <dc:identifier>doi:10.1016/j.envres.2024.119007</dc:identifier>
  1004.    </item>
  1005.    <item>
  1006.      <title>Increase in Functional Tic Presentations in Sexual Orientation and Gender Identity Minority Youth During Coronavirus Disease 2019</title>
  1007.      <link>https://pubmed.ncbi.nlm.nih.gov/38677240/?utm_source=Feedvalidator&amp;utm_medium=rss&amp;utm_campaign=None&amp;utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&amp;fc=None&amp;ff=20240501180032&amp;v=2.18.0.post9+e462414</link>
  1008.      <description>CONCLUSIONS: Our data confirm previously demonstrated dramatic rises in functional tic presentations during the COVID-19 pandemic and, more notably, reveal a strong association with SOGI minority status. We highlight the potential link between functional tic disorders and SOGI minority status. Providing a safe and supportive clinical environment and addressing stress linked to SOGI minority status may help to improve patient prognosis.</description>
  1009.      <content:encoded><![CDATA[<div><p style="color: #4aa564;">Pediatr Neurol. 2024 Apr 5;155:182-186. doi: 10.1016/j.pediatrneurol.2024.03.027. Online ahead of print.</p><p><b>ABSTRACT</b></p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">BACKGROUND: Functional tic disorders are among the least common functional movement disorders, but their prevalence rose during the coronavirus disease 2019 (COVID-19) pandemic. Although female adolescents develop functional neurological disorders at higher rates than males, investigations into sexual orientation and gender identity (SOGI) status of these patients are limited.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">METHODS: We completed a retrospective, cross-sectional time series examining the incidence of new-onset functional tic disorders in youth presenting to the Massachusetts General Hospital Movement Disorder clinics before and during the COVID-19 pandemic. Data were collected by searching for relevant International Classification of Diseases (ICD)-10 diagnostic codes in youth aged nine to 26 years using a hospital-wide data repository. Individual cases were reviewed for inclusion based on clinical criteria and expert consensus.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">RESULTS: The prevalence of functional tic presentations in youth rose 8.6-fold from pre- to postpandemic levels (Fisher exact test P &lt; 0.001), whereas the prevalence of developmental tic presentations pre- and postpandemic remained stable (114 vs 112). SOGI minority youth comprised 37% of those with functional tics (total n = 19). Ninety five percent of patients with functional tics identified as female, with 10% of these identifying as transgender.</p><p xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:p1="http://pubmed.gov/pub-one">CONCLUSIONS: Our data confirm previously demonstrated dramatic rises in functional tic presentations during the COVID-19 pandemic and, more notably, reveal a strong association with SOGI minority status. We highlight the potential link between functional tic disorders and SOGI minority status. Providing a safe and supportive clinical environment and addressing stress linked to SOGI minority status may help to improve patient prognosis.</p><p style="color: lightgray">PMID:<a href="https://pubmed.ncbi.nlm.nih.gov/38677240/?utm_source=Feedvalidator&utm_medium=rss&utm_content=1vGIiL00qKe440DIRc4MaFKgmUECUPeuTJc1vQeV37XLxuBgYv&ff=20240501180032&v=2.18.0.post9+e462414">38677240</a> | DOI:<a href=https://doi.org/10.1016/j.pediatrneurol.2024.03.027>10.1016/j.pediatrneurol.2024.03.027</a></p></div>]]></content:encoded>
  1010.      <guid isPermaLink="false">pubmed:38677240</guid>
  1011.      <pubDate>Sat, 27 Apr 2024 06:00:00 -0400</pubDate>
  1012.      <dc:creator>Amy Armstrong-Javors</dc:creator>
  1013.      <dc:creator>Evan Realbuto</dc:creator>
  1014.      <dc:creator>Marisela E Dy-Hollins</dc:creator>
  1015.      <dc:creator>Jeremiah M Scharf</dc:creator>
  1016.      <dc:date>2024-04-27</dc:date>
  1017.      <dc:source>Pediatric neurology</dc:source>
  1018.      <dc:title>Increase in Functional Tic Presentations in Sexual Orientation and Gender Identity Minority Youth During Coronavirus Disease 2019</dc:title>
  1019.      <dc:identifier>pmid:38677240</dc:identifier>
  1020.      <dc:identifier>doi:10.1016/j.pediatrneurol.2024.03.027</dc:identifier>
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