Not All Bad? APOE4 Sharpens Memory in Older People
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.
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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.
Bumetanide normalizes molecular signatures linked to the AD risk allele. People taking the medicine may be less likely to develop Alzheimer’s.
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.
The AD risk allele steers microglia toward an inflammatory state long before plaques or tangles emerge.
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.
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.
The academy elected 90 new members. Five are well-known for their contributions to the field of neurodegenerative diseases.
The SARS-CoV2 spike and other viral glycoproteins promote the transmission of proteopathic seeds carried by extracellular vesicles.
In tau knockout mice, excitatory neurons fire less; inhibitory neurons fire more. Could this dampen hyperexcitability in conditions such as Alzheimer’s?
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?
Microglia regurgitate tau seeds. Then they retreat into a senescent torpor. In this state, they nonetheless pump out potentially hazardous metalloproteases.
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.
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.
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.
At a recent conference, researchers presented more evidence tying the APOE4 allele to disrupted lipid metabolism. They linked this problem to Aβ production.