‘Cartoonishly oversimplistic’: Researchers rethinking amyloid hypothesis for Alzheimer’s

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[Experts are] divided about whether treating amyloid buildup—long thought to be the best target for an Alzheimer’s therapy—is still a promising approach.

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.

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.

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