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.
Early data suggest that CT1812 and AL001 shift biomarker levels in Alzheimer’s disease and frontotemporal dementia, respectively. BI 425809 fails to improve cognition.
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.
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.
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.
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.
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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.
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.