Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
Three studies found no link between vascular disease and cerebral amyloidosis.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In Alzheimer’s brain, granulovacuolar bodies in neurons harbor activated necrosomes. They correlate with tau pathology and neuron loss, raising new questions about how neurons die in this disease.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
Data from different next-generation tracers look similar. It shows spreading plaques kick off tangles by Braak region; memory starts slipping later.
NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019 ...
Happy New Year, readers! Yes, 2019 has passed, but so much happened last year that capturing the essence took longer than usual. Our mega year-end story is now posted for your reading pleasure.
A half-dozen lesser-known compounds in trials for Alzheimer’s disease posted results at the CTAD conference.
Bringing the total NIH funding for Alzheimer’s research up to $2.8 billion, the Senate continued its steady upward climb in spending for the disease.
Apabetalone, an epigenetic drug that tamps down vascular inflammation, slowed cognitive decline in people with MCI. A new statistical analysis of results from AMBAR claimed the plasma-exchange therapy might boost cognition by removing pathogenic proteins from blood.
At CTAD, researchers discussed possible paths forward. One option: exploring whether low doses prevent plaque accumulation while avoiding the cognitive side effects.
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.