Better Cell Model? Transdifferentiated Neurons Capture AD-Like Changes
New studies report that transdifferentiated neurons from AD patients retain signatures of aging. They also model lysosomal dysfunction, tau phosphorylation, and cell death.
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New studies report that transdifferentiated neurons from AD patients retain signatures of aging. They also model lysosomal dysfunction, tau phosphorylation, and cell death.
Cells of the neurovascular unit upregulate inflammation-related genes and stifle genes of the blood-brain barrier. The genes include 125 known to carry AD risk variants.
Feeding taurine to mice and monkeys increased the lifespan of the former and reduced signs of aging in both.
Known for his work on animal models, APP processing, and the cholinergic system, Price founded one of the first Alzheimer’s Disease Research Centers.
In cognitively unimpaired older adults, some gut bacteria correlated with plaques and tangles, but not neurodegeneration.
A giant of basic science, Ihara biochemically characterized Aβ and tau deposits in AD brain, laying the groundwork for subsequent discoveries.
The panel was persuaded of the antibody’s clinical efficacy and overall favorable benefit/risk ratio, although it had questions about risk in certain subgroups.
In VSP35 knockout cells, surface proteins get trapped in endolysosomes. They swell with undigested proteins and APP, then spew their contents outside the cell.
In amyloidosis mice, decline of the hypothalamic melanin-concentrating hormone system jacks up neuronal activity, and contributes to sleep problems.
A tiny PET study saw gliosis in putamen and striatum of some with persistent depression after COVID; larger health registry studies find scant evidence.
Dozens of structural features of the heart correlated with measures of regional volume, integrity of white-matter tracts, and functional connectivity within the brain.
The agency reiterated its earlier decision that traditionally approved amyloid antibodies will be covered if physicians enter data into a patient registry.
Among cognitively healthy people, amyloid load tracked with blood p-tau181 and tangles only in those with high blood GFAP.
Backed up, the cells never transitioned into a disease-associated state, shirking their plaque compaction and synapse protection duties.
Three reviews, two perspectives, and four comments discuss recent advances and opportunities for dementia research.
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