Can BACE2 Protect Against Amyloidosis?
The protease suppresses Aβ in Down’s syndrome organoids.
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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.
A GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.
As the SARS-Cov-2 infection peak passes in some areas, scientists are resuming lab work and clinical studies, albeit with new safety protocols in place. Regions differ greatly in how fast they can reopen.
A 2018 report that had spotted extra copies of APP lurking in neuronal genomes has come under scrutiny, with claims that the result is due to contamination. Does a response from the original authors bolster their claim?
This neuronal protein regulates the complement cascade in the developing brain. Could it do the same in aging or neurodegenerative disease?
Carriers accumulate fewer tangles than noncarriers for a given amount of amyloid, explaining how the gene variant may lower a person’s Alzheimer’s risk.