α-Synuclein Spurs Neuroinflammation Via Microglial LRRK2
The transcription factor NFATc2 mediates this response.
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The transcription factor NFATc2 mediates this response.
By looking for SNPs that affect how transcription factors bind DNA, researchers nominated causal genes for 30 Alzheimer’s and Parkinson’s GWAS hits.
A new single-nucleus RNA-Seq study of 3,900 endothelial cells finds a boost in angiogenesis and antigen presentation genes, drawing attention to the vascular component of AD.
In a retrospective study, people with vitiligo had 12 times the risk of developing Alzheimer’s disease than did healthy controls. Why is that?
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.
The day-long advisory committee meeting will be broadcast live online. Prerecorded presentations are to be available November 4; the public can submit comments.
A recent genetics symposium drew positive reviews for its approach of following up prerecorded, on-demand talks with a live Q&A session.
Two papers report that skin samples from people with Parkinson’s disease contain α-synuclein seeds that can be robustly amplified, paving the way for a reliable test for the disease.
Reducing levels of monounsaturated fatty acids lowered α-synuclein toxicity and prevented movement symptoms in mice. Scientists say the data boost the α-synuclein tetramer hypothesis.
Armed with snazzy new hardware, scientists solve protein structures to a resolution of 1.22Å. Cryo-EM now rivals X-ray crystallography.
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.
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 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.