Just to give most everyone in the Alzheimer’s field a little more reason to doubt themselves, the Mayo Clinic has published a study suggesting that the pathology associated with tau protein (neurofibrillary tangles, NFT) is (as some have always maintained) more important than that associated with beta-amyloid.
Our observations reaffirm the concept that amyloid-β burden itself is not the proximate causal pathology for cognitive decline. . .Abnormal accumulation of amyloid-β and NFT pathology likely occurs in parallel with one another, eventually resulting in incompletely understood crosstalk between the pathologies. . .Although cortical accumulation of amyloid-β was considered sufficient to influence the risk of clinical Alzheimer’s disease, we and others demonstrate that NFT accumulation mediates the contribution of amyloid-β pathology to cognitive decline.
This won’t settle the argument, by any means, but it is more food for thought for the many organizations targeting amyloid itself. It’s always possible that (because of the crosstalk mentioned above) that amyloid-centric approaches could still be of benefit (just as it’s possible that amyloid still is the real driver of the disease state). But neither of these are sure things. Alzheimer’s has no sure things.