![[Valid RSS]](images/valid-rss-rogers.png "Valid RSS")
This is a valid RSS feed.
This feed is valid, but interoperability with the widest range of feed readers could be improved by implementing the following recommendations.
[help]
<rss version="2.0" xmlns:prism="http://purl.org/rss/1.0/modules/prism/">
line 17, column 6: (4 occurrences) [help]
<prism:startingPage xmlns:prism="prism">awaf417</prism:startingPage>
^
</channel>
^
<?xml version="1.0"?><rss version="2.0" xmlns:prism="http://purl.org/rss/1.0/modules/prism/"> <channel> <title>Brain Advance Access</title> <link>http://academic.oup.com/brain</link> <description> </description> <language>en-us</language> <pubDate>Tue, 04 Nov 2025 00:00:00 GMT</pubDate> <lastBuildDate>Mon, 03 Nov 2025 19:46:05 GMT</lastBuildDate> <generator>Silverchair</generator> <item> <title>Sex-dependent effects of maternal high-fat diet during lactation in the offspring of adult THY-Tau22 mice</title> <link>https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awaf417/8313596?rss=1</link> <pubDate>Tue, 04 Nov 2025 00:00:00 GMT</pubDate> <description><span class="paragraphSection"><div class="boxTitle">Abstract</div>The perinatal environment has been suggested to participate in the development of tauopathies and Alzheimer’s disease but the molecular and cellular mechanisms involved remain contradictory and under-investigated. Here, we evaluated the effects of a maternal high-fat diet (HFD) during lactation on the development of tauopathy in the THY-Tau22 mouse strain, a model of progressive tau pathology associated with cognitive decline.During lactation, dams were fed either a chow diet (13.6% of fat) or a HFD (58% of fat). At weaning, offspring were fed a chow diet until sacrifice at 4 months of age (the onset of tau pathology) or 7 months of age (the onset of cognitive impairment).During lactation, maternal HFD increased body weight gain in offspring. At 3 months of age, maternal HFD led to a mild glucose intolerance only in male offspring. Moreover, it impaired spatial memory in both male and female 6-month-old offspring, with males being more impacted. These cognitive deficits were associated with increased phosphorylation of hippocampal tau protein-observed at 4 months in males and at 7 months in females, highlighting a sex-specific temporal shift. Additionally, maternal HFD modified adult hippocampal neurogenesis (AHN), leading to an increase of mature neuronal cells number in females and of dendritic arborization length in males. Synaptic analysis further revealed that maternal HFD led to synaptic loss only in males. Finally, multi-omics approaches showed that maternal HFD has long-term consequences on both transcriptome, proteome and regulome, this effect being also sex-dependent with mitochondrial pathways, ribosomal activity, cilium and the extracellular matrix predominantly impacted in males, while gliogenesis, myelination and synaptic plasticity were primarily affected in females. Regulome analysis suggested that this sex-dependent phenotype was more related to a temporal shift rather than distinct sex-specific alterations. Collectively, our data suggest that maternal HFD accelerates the development of tauopathy in THY-Tau22 offspring, with sex-dependent effects, males being impacted earlier than females. These findings highlight that exposure to maternal HFD represents a critical window of vulnerability, and potentially of opportunity, for interventions aimed at preventing the development of neurodegenerative diseases.</span></description> <prism:startingPage xmlns:prism="prism">awaf417</prism:startingPage> <prism:doi xmlns:prism="prism">10.1093/brain/awaf417</prism:doi> <guid>http://doi.org/10.1093/brain/awaf417</guid> </item> <item> <title>Estimating the time course of biomarker changes in Alzheimer’s disease</title> <link>https://academic.oup.com/brain/advance-article/doi/10.1093/brain/awaf413/8313033?rss=1</link> <pubDate>Mon, 03 Nov 2025 00:00:00 GMT</pubDate> <description><span class="paragraphSection"><div class="boxTitle">Abstract</div>Recent advancements in biomarkers have transformed Alzheimer’s disease (AD) diagnosis from being purely symptom-based to include biological criteria. With new treatments targeting AD’s core biology, understanding the timeline of biological changes is crucial as the disease progresses over decades.Longitudinal data from amyloid-beta (Aβ) PET and cognitive tests (MMSE and ADAS-cog) from the Alzheimer’s Disease Neuroimaging Initiative (n=1,448) and BioFINDER (n=2,088) were used to stage patients against an estimated continuous disease timeline (predicted time since Aβ-PET positivity). The estimated timeline was validated by comparing correlations with unseen biomarkers and cognitive measures against alternative staging approaches. Trajectories for plasma, CSF, MRI, and PET biomarkers, measuring Aβ, tau, and neurodegeneration, were mapped along this AD continuum.The proposed staging approach was found to produce stronger correlations with unseen cognitive measures and biomarkers compared to alternative staging methods, including amyloid and tau PET clocks (all pairwise p&lt;0.05). Findings related to biomarker trajectories were highly consistent across cohorts. The period from Aβ-PET positivity to end-stage AD dementia (MMSE = 0) was estimated at 20-25 years, with a presymptomatic phase of 7-11 years. CSF Aβ42/40 became abnormal about a year before Aβ-PET positivity, CSF p-tau231, p-tau217, and plasma p/np-tau217 1-3 years after, and tau-PET about 8 years after. Neurodegenerative biomarkers, such as hippocampal volume, became clearly abnormal in early dementia stages, 14-16 years after Aβ-PET positivity.The progression from initial biomarker abnormality to severe AD spans two decades. Disease progression modeling elucidates the evolution of AD biomarkers and cognition, highlighting the relative timing of biomarker abnormalities. These models can determine disease stages, aiding prognosis and evaluation for disease-modifying treatments.</span></description> <prism:startingPage xmlns:prism="prism">awaf413</prism:startingPage> <prism:doi xmlns:prism="prism">10.1093/brain/awaf413</prism:doi> <guid>http://doi.org/10.1093/brain/awaf413</guid> </item> </channel></rss>If you would like to create a banner that links to this page (i.e. this validation result), do the following:
Download the "valid RSS" banner.
Upload the image to your own server. (This step is important. Please do not link directly to the image on this server.)
Add this HTML to your page (change the image src attribute if necessary):
If you would like to create a text link instead, here is the URL you can use:
