At AAN, the latest data from Phase 3 trials and open-label extensions of RNA-targeting therapies reveal a bit of benefit, but no cure.
Genetic adaptations that gave humans their smarts may promote diseases of aging, including cancer, Alzheimer’s, and Parkinson’s. One adaptation counteracted REST, a proposed protector against AD.
High vascular risk scores and Aβ burden independently associate with cognitive decline, but combined, they speed things up.
Prior evidence for protective effect evaporates after adjustment for demographic differences in high- and low-lithium communities.
PET study finds tau signal associated with markers of cerebrovascular disease and cognitive issues.
Not the brown trucks with the friendly delivery guys: UPS as in unconventional protein secretion pathway. Tau rides it to slink out of one cell, and, grabbing onto heparin sulfate proteoglycans, enter another.
The company has halted all trials of atabecestat.
Engineered nanoparticles snatched extracellular Aβ, ferried it into cells, and switched on autophagy, clearing the peptide from the brains of mice. Would this work as a drug?
Contrary to previous findings, both proteins seem to escape via passive diffusion. This has implications for therapeutic strategies to keep them where they belong.
Aggregates that form inside, or just pass through, oligodendrocytes take on the properties of the virulent strain that gives rise to multiple system atrophy.
ApoE4 raises CSF tau more in women than in men, suggesting sex may influence the risk of neurodegeneration, especially in amyloid-positive E4 carriers.
Exposure to lipid membranes embedded with cholesterol accelerate Aβ fibril formation by up to 20-fold.
A large retrospective study in veterans finds that even brain injuries that cause no loss of consciousness come with a twofold higher risk of developing all-cause dementia.
The two datasets reveal almost identical cognitive decline in prodromal AD, the stage targeted by secondary prevention trials.
Even at below threshold levels, cortical amyloid can drive cognitive decline, tau accumulation.
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