First Primate Model of Familial AD: Marmosets with Presenilin Mutation
Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
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Three young monkeys missing exon 9 of presenilin 1 seem to have an elevated Aβ42/40 ratio. It remains to be seen if they will develop plaques and tangles as they age.
While gene-based therapy for late-onset AD may seem distant, rare neurological disorders could point the way.
A small molecule binds the retromer complex, preventing Aβ accumulation, tau hyperphosphorylation, and their downstream consequences in mice.
Quite independently of what it does to Aβ or tau, ApoE4 stokes α-synuclein pathology in mouse models. People with Lewy body dementia who carry ApoE4 had more phosphorylated synuclein in their brains, and their cognition declined faster.
Post-translational modifications differ from those in AD tau fibrils, and may dictate tau strains.
The protease suppresses Aβ in Down’s syndrome organoids.
Centenarians who scored high on the MMSE stayed cognitively and physically active over the next two years, even if they carried genetic risk factors for Alzheimer’s. What protects these lucky few?
The slowdown of proteasomes stymied TDP-43’s entry into the nucleus and promoted its aggregation in the cytoplasm.
Massive meta-analysis finds the longevity gene’s VS haplotype staves off mild cognitive impairment and AD. It reduces amyloid burden.
Grown on doughnut-shaped supports, the cultures survive for years. They offer a versatile system for studying Alzheimer’s disease, the authors claim.
This update of the Allen Brain Institute atlas reveals detailed anatomical structures and provides a common framework for comparing brain datasets.
Separately, cerebrovascular disease drove an uptick in neurofilament light in the brain, indicating neurodegeneration.
The plasma biomarker neurofilament light was able to distinguish individual mutation carriers from noncarriers three years prior to onset.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
Researchers identify a way to isolate human astrocytes generated from induced pluripotent stem cells. And astrocytes stand out in FTD-prone brain areas.