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According to [geneticist John] Hardy, who runs a molecular neuroscience program at University College London’s Institute of Neurology, “the [concept] we drew in 1998 is cartoonishly oversimplistic. There were lots of question marks. We thought those questions would be filled in within a couple of years. And yet 20 years later they are not filled in.” Other experts, though, still contend that the amyloid hypothesis is a strong explanation and that treatments targeting the protein are the right way to go.
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Some researchers, such as Karen Duff of Columbia University, favor the idea that tau protein tangles play a part that is as big as or bigger than that of beta-amyloid. One reason is that the degree of tau pathology more closely correlates with the seriousness of cognitive symptoms than amyloid pathology does.
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Going forward, it seems unlikely that the field will abandon the amyloid hypothesis. But scientists do seem, after a long time, poised to take a broader view of other processes at work in this destroyer of minds and memories.
