New study finds no uptick in herpes viruses in AD. If herpes plays a role, it says, then probably it acts as an early trigger of pathology.
Single-nucleus transcriptomics of postmortem AD brain and mouse models of amyloidosis hammers home the species-specific responses of microglia to Aβ pathology.
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.
Aβ oligomers latch onto adrenergic receptors, mobilizing a kinase that phosphorylates tau. Blocking adrenergic signaling wards off memory problems in amyloidosis mice.
The cells are primed to attack. Their targets include Epstein-Barr virus peptides.
Three studies found no link between vascular disease and cerebral amyloidosis.
A half-dozen lesser-known compounds in trials for Alzheimer’s disease posted results at the CTAD conference.
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.
NIH Summit Sets Agenda for AD-Related Dementias Alzheimer's Disease Research Summit 2019 ...
Besides further broadening the Alzheimer’s therapeutic pipeline, researchers urge a return to Phase 2, using artificial intelligence tools to streamline aspects of trials.
Positive allosteric modulators improve learning and memory in mouse models of AD and epilepsy.
In early Alzheimer’s disease, the pattern of tau deposition also strongly predicts areas destined for subsequent degeneration.
These oily microglia resemble the foamy macrophages seen in atherosclerotic plaques. They correlate with aging, inflammation, and neurodegenerative disease.
Data from different next-generation tracers look similar. It shows spreading plaques kick off tangles by Braak region; memory starts slipping later.