This isn’t the first paper I’ve seen to argue the point that there should be a greater focus on tau aggregation in Alzheimer’s disease, and that tau may be more important to the progression of the condition. As I’m sure the readers here are aware, Alzheimer’s is characterized by the buildup of both amyloid-β and tau in the brain. Forms of these normally soluble proteins precipitate into solid deposits that are accompanied by a complex halo of biochemistry that degrades the function of neurons and ultimately kills these cells. The primary focus for development of therapies has long been the removal of amyloid-β, but despite enormous effort there is no light at the end of the tunnel yet. The history of clinical trials for amyloid-β clearance is one of unremitting failure, even recently in trials that produced evidence for amyloid-β to be removed to some degree in patients.
It is much debated as to whether trials are failing because amyloid-β is the wrong target, despite being harmful in and of itself, or because Alzheimer’s is a hard problem. Alzheimer’s research has proceeded in parallel with mapping the
Article originally posted at