While the FDA weighs aducanumab’s marketing license application, Alzheimer’s researchers agree that the agency’s own statistician correctly assessed the data as weak. Most prefer that one more trial be done.
After years of building an online registry, designing selection algorithms, and getting sites up and running, COVID-19 nearly derailed this trial-ready cohort once again. Now, the first participants have reached the final queue.
The anti-Aβ biologic will be put to the test in two stages of preclinical Alzheimer’s, designated by amyloid load. The long-dormant “est” PET tracer, NAV4694, is on board to make sensitive measurements.
At CTAD, a Phase 2 open-label extension of this anti- Aβ protofibril antibody posted data as expected, and new Phase 3 trials for people with early and preclinical Alzheimer’s were described.
BANish Aβ? BAN2401 Antibody Makes Its Move in Phase 3 Program BAN2401 Forges AHEAD into Phase 3, Preclinical AD TRC-PAD Funnel Finally Touches Down Learning Troubles Spied by Smartphone Track with Biomarkers In Phase 2 Trial, Neflamapimod Aids Cognition ...
Could this forestall the amyloid cascade and the onset of Alzheimer’s disease?
In mice, accumulation of tau in hilar astrocytes of the dentate gyrus spells trouble for the hippocampus and for spatial memory.
The panel considered the evidence for efficacy to be weak, and was troubled by too-close collaboration between the sponsor and the FDA.
In a mouse model of ALS, removing mutant SOD1 from peripheral myeloid cells relieved neuroinflammation and extended lifespan.
Simple lifestyle factors such as alcohol consumption and stool quality alter gut flora. Research on the microbiome and disease should account for those factors, a study reports.
The transcription factor NFATc2 mediates this response.
ApoE4 does so much more strongly than the other known genes collected in a polygenic risk score.
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.
The first steps of endocytosis faltered in astrocytes expressing ApoE4, but pumping in PICALM reversed the problem. A new study places two Alzheimer’s risk factors into the same cellular mechanism.
Three amino acid substitutions in the Aβ sequence accelerate BACE cleavage of APP and ramp up Aβ production in rats and mice. The mice can serve as better controls for mutant APP knock-ins already in use.