Regulators in the U.S. and Europe have certified a mass-spectrometry-based blood test for amyloid-β. Plasma phospho-tau markers are poised to come next.
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.
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.
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.
Researchers identify a way to isolate human astrocytes generated from induced pluripotent stem cells. And astrocytes stand out in FTD-prone brain areas.
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 GWAS of co-expression modules identifies a haplotype that disrupts lysosomes and myelination. ApoE4 and Aβ regulate the same module.
Post-translational modifications differ from those in AD tau fibrils, and may dictate tau strains.
The protease suppresses Aβ in Down’s syndrome organoids.