A SARS-CoV-2 protease cleaves the transcription factor NEMO, which protects the brain's endothelial cells. In people who had COVID, and mice lacking NEMO, blood vessels shriveled. Could long COVID increase risk for dementia?
In tau knockout mice, excitatory neurons fire less; inhibitory neurons fire more. Could this dampen hyperexcitability in conditions such as Alzheimer’s?
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.
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.
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.
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.