The SARS-CoV2 spike and other viral glycoproteins promote the transmission of proteopathic seeds carried by extracellular vesicles.
The academy elected 90 new members. Five are well-known for their contributions to the field of neurodegenerative diseases.
In a tiny Phase 3 trial of the ASO tofersen, a neurodegeneration marker changed in the right direction. Trends on other endpoints favored drug. Still, the trial was negative. Next steps for tofersen remain up in the air.
In Lewy body dementia brain tissue, CD4+ T cells loitered near synuclein aggregates and dopaminergic neurons. In vitro, T cells reacted to α-synuclein fragments by spewing the pro-inflammatory cytokine interleukin 17A.
An analysis suggests most Medicare beneficiaries have medical conditions that would disqualify them from using the new drug; this may further limit its clinical rollout.
Eisai/Biogen file for accelerated approval of lecanemab based on Phase 2 data. Eli Lilly likely to do the same for donanemab this year.
The AD risk allele steers microglia toward an inflammatory state long before plaques or tangles emerge.
A new study reports that activated microglia soak up glucose, and may be responsible for the elevated FDG PET signal seen in early Alzheimer's disease. Mouse microglia used 28 times more FDG than did neurons.
Bumetanide normalizes molecular signatures linked to the AD risk allele. People taking the medicine may be less likely to develop Alzheimer’s.
Cognitively intact 70-year-old people carrying APOE4 recalled objects and their locations slightly better than did noncarriers. The advantage persisted even among people who had amyloid plaques.
That long-sought astrocyte toxicity factor? Scientists say it's certain long-chain fatty acids. No, not the ones we get from our diet.
In a collaborative tour de force, scientists for the first time compared eight Aβ assays in the same plasma samples. Mass-spectrometry assays more accurately picked up brain amyloid than did most immunoassays, but one fully automated immunoassay was on par.
High-resolution structures of tau fibrils from a variety of tauopathies reveal distinct folds—and important similarities—among syndromes. The folds facilitate a classification of tauopathies.
Therapies targeting key neurodegenerative disease proteins, or biomarkers, are failing. Can Mendelian randomization test cherished assumptions?
The APOE3-Jacksonville variant generates a protein whose greater lipid-hauling capacity renders it less prone to self-aggregate. This boosted phospholipid trafficking and reduced the number of plaques and downstream damage.
No filters selected