The FDA will decide whether to approve the antibody as a treatment for Alzheimer’s disease on or before March 7, 2021.
Three weeks of on-demand seminars to culminate in live Q&A.
Restoring proper gene editing assuaged mitochondrial defects in patient-derived neurons and organoids. Splicing errors may underlie other PD cases as well.
Poor coordination among grid cells in the entorhinal cortex and place cells in the hippocampus compromises navigation. Grid cells fail first.
New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
New synaptic profiling and imaging techniques are enabling scientists to zero in on synaptic proteins, including phospho-tau, that make the difference between clinical Alzheimer’s and resilience.
New genetic variants emerged by harmonizing whole-exome-sequencing data across continents, and by using imputation to plumb the depths of existing GWAS. One variant encodes a microglial phospholipid transporter.
At AAT-ADPD, researchers report how they built on prior reports that a person’s blood level of p-tau181 tells if they have Alzheimer’s.
The first topline Phase 2 results from an antibody targeting Parkinson’s pathology, Roche’s prasinezumab, were a mixed bag. Next steps are unclear.
Plaque-busting antibodies reset the time course of amyloid accumulation, but so far provide only hints of a clinical benefit in mild AD. Good news: once gone, plaque stays gone for a while.
Subtle memory deficits resolved after volunteers stopped taking the Novartis BACE inhibitor.
Researchers used PET scans from 4,000 people to link RBFOX1 risk variants to amyloidosis. People with lower RBFOX1 expression in their brains had more amyloid and worse cognition.
Negative findings for AVP-786 belie positive findings from a separate Phase 3 trial announced earlier this year.