In mouse models, a sluggish thalamic reticular nucleus shortens slow-wave sleep. In one model, activating this brain area lengthened the mice's slumber while also reducing their plaque loads.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.
Having a serious flu upped a person's odds of getting PD a decade later; a sedentary life dimmed prospects of living with PD; and cerebrovascular pathology implied more severe parkinsonism. Deaths due to PD have risen in the United States.
A paper marrying math modeling with biological data proposes that, past Braak Stage III, tau aggregates double every five years in the neocortex. By this stage, they were already distributed throughout, de-emphasizing spread.
A combination of retinoic acid and the cholesterol drug gemfibrozil prompted astrocytes to ingest and degrade Aβ. Mice treated this way had fewer amyloid plaques and performed better on cognitive tests.
Microglia regurgitate tau seeds. Then they retreat into a senescent torpor. In this state, they nonetheless pump out potentially hazardous metalloproteases.
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?
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.
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