Early dysfunction in Alzheimer’s may start in the lateral entorhinal cortex and spread from there to connected cortical brain regions.
By stopping familial amyloid polyneuropathy in its tracks, a repurposed anti-inflammatory medication supports the idea that artificial chaperones can prevent protein aggregation.
Researchers at BACE meeting explore how trafficking and degradation of the protease relate to amyloid pathology in AD.
In neurodegenerative disease, tau is in the dendrites, and scientists are beginning to flesh out ways to block what it does there.
New research suggests that TDP-43 attacks neurons by deactivating a translation initiation factor. Keeping the factor active holds toxicity at bay in flies.