New drug application is first for Alzheimer’s disease in the U.S. since 2003, and first based on amyloid hypothesis.
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.
In a conditional mouse knockout, lack of neuronal BIN1 slowed excitatory signaling, leading to spatial memory problems. Could this play a role in Alzheimer’s?
Phospholipase C-γ2 acts downstream of TREM2 to rev up beneficial inflammation, phagocytosis, and cell survival.
The modeling approach reinforces the idea that tau pathology propagates through the brain’s physical architecture, including neuronal networks.
Data shown at AAT-AD/PD explain why the DIAN-TU trial missed its primary endpoint. But gantenerumab strongly reduced plaques, tau, phospho-tau, and slowed NfL. This result prompted an open-label extension, sustaining hope for efficacy.
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.
In a career spanning four decades, Davies spearheaded the cholinergic hypothesis, unlocked secrets of tau, and readily shared antibodies in the field.
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.
New genetic variants emerged by harmonizing whole-exome-sequencing data across continents, and by using imputation to plumb the depths of existing GWAS. One variant encodes a microglial phospholipid transporter.