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A new study is changing how scientists think about Alzheimer’s disease

How does ApoE4 do its dirty work? Since 1993, when this variant of the apolipoprotein E gene was found to multiply the risk of the most common form of Alzheimer's disease as much as fourfold, researchers have probed its connections to β-amyloid, the dominant suspect for the cause of the illness. This protein fragment forms extracellular "plaques" that can disrupt brain signals and kill neurons. This week, however, one of the main proponents of the hypothesis that ApoE4exacerbates amyloid pathology stunned many of his colleagues by showing that its most toxic effects may result from a damaging immune response to a different protein: tau.

"This is a seminal study" and has "profound clinical implications," says Bob Vassar, a molecular biologist at Northwestern University in Chicago, Illinois. The study also shifts the terms of an old debate over whether Alzheimer's treatments should focus on tau or amyloid, by suggesting both could be targeted through ApoE4. Because David Holtzman, the leader of the new study, has long championed a link between ApoE4 and β-amyloid, "it's very compelling to hear him argue now" that tau is central to ApoE4's dangerous influence, says Scott Small, a neuroscientist at Columbia University.

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Written by Emily Underwood for


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