A protein called Arc appears to act as a courier for toxic Tau, carrying it from sick brain cells into healthy ones, according to researchers at University of Utah Health working in mice. Tau buildup kills neurons, and as the damaged protein spreads through the brain, symptoms worsen and eventually become fatal - so identifying what moves it from cell to cell has been a long-standing question in Alzheimer's research.
The practical appeal here is that spread, rather than the initial damage, may be the more tractable target. Most people are diagnosed after Tau pathology is already established in part of the brain. A treatment that interrupted the hand-off between neurons would not undo existing damage, but it could in principle keep the disease from marching into new regions and taking more cognitive function with it.
"I'm excited by the fact that we've identified a new way of potentially stopping the progression of Alzheimer's disease," said Jason Shepherd, PhD, professor of neurobiology at University of Utah Health and the study's senior author.
This is mouse work, and the gap between a mechanism identified in animals and a drug that helps patients is a wide one. Still, the finding gives researchers a specific molecular player to aim at, which is a more concrete starting point than the broad goal of clearing Tau after it has already accumulated.