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Volume 575 Issue 7784, 28 November 2019

Twisted tale

The cover image shows tau protein (blue) accumulating inside neurons. Alongside amyloid-β, tau is believed to play a significant part in Alzheimer’s disease. Whereas amyloid-β accumulates in plaques, hyperphosphorylated tau aggregates in neurofibrillary tangles; these plaques and tangles contribute to neurodegeneration and cognitive decline. Activation in microglia of the NLRP3 inflammasome, a protein complex that is part of the body’s natural defences, is essential for amyloid-β plaque formation. In this week’s issue, Michael Heneka and his colleagues reveal that the NLRP3 inflammasome also helps to drive the formation of tau tangles. The team shows that tau tangles develop downstream of amyloid-β activating microglia and the NLRP3 inflammasome, lending support to the amyloid-cascade hypothesis in Alzheimer‘s disease. The researchers also find that tau itself can prompt activation of the inflammasome, hinting that there may be broader implications for other neurodegenerative diseases.

Cover image: Pixeldust Studios

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