Longitudinal neuroimaging of DIAN participants reveals that in most regions of the brain affected by AD pathology, Aβ accumulates first, then metabolism slows, then the brain shrinks.
The PDE9A inhibitor BI 409306 failed to improve cognition in Phase 2 trials.
A variant squelching expression of PAD4 enzyme reportedly drives up ALS risk by reducing aggregation of RNA-binding proteins.
First presented at CTAD 2017, results suggest good safety, hint at efficacy for this serotonin-targeted drug.
Its Challenge Network seeks to attract new investigators and new ideas to focus on cross-disease cell biology.
The Italian biochemist was part of the team that identified tau as the major component of neurofibrillary tangles in 1985.
Researchers claim that amyloid deposits completely vanish when BACE1 expression is gradually shut down in adult, plaque-ridden mice.
Two transcriptional profiles of astrocytes in healthy old mice record a surge in reactive and inflammatory gene expression.
Newly found labile cross-β filament structures may mediate multivalent protein interactions among low-complexity domains.
A meta-analysis confirms microglial phenotypes associated with neurodegeneration, but highlights differences between human and mouse.
Researchers improve word recall by jolting the lateral temporal cortex, claiming this counters firing patterns linked to poor memorization.
Healthy people with Aβ buildup have irregular circadian rhythms. In mice, circadian disruptions dull daily Aβ oscillations and lead to more plaques.
The Phase 3 APECS trial of Merck’s flagship BACE inhibitor ends prematurely following an interim safety analysis.
In people with an autosomal-dominant AD mutation, Aβ and tau start accumulating long before the estimated onset of symptoms.
Knocking down these capillary-hugging cells triggers a domino effect; blood proteins invade the brain, white matter deteriorates, and neurons die.