Dementia in Alzheimer’s May Result from Dual Blow to Brain: Amyloid Clumps and Tau Tangles

Dementia in Alzheimer’s May Result from Dual Blow to Brain: Amyloid Clumps and Tau Tangles
Amyloid-β plaques accumulating in the brain alone are not enough to cause the dementia that characterizes Alzheimer’s, new research from Johns Hopkins University argues. Instead, a second blow — molecular pathways that ultimately cause tau proteins to form tangles inside nerve cells — is also needed for neurons to degenerate. The study, The neuritic plaque facilitates pathological conversion of tau in an Alzheimer’s disease mouse model, published on Monday in the journal Nature Communications, might debunk the notion that amyloid-β plaques are disease-causing in their own right. "For the first time, we think we understand that the accumulation of amyloid plaque alone can damage the brain, but that's actually not sufficient to drive the loss of nerve cells or behavioral and cognitive changes," said Philip C. Wong, a professor of pathology at the university's School of Medicine, in a press release. "What appears to be needed is a second insult — the conversion of tau — as well." The two processes — aggregation of amyloid-β into clumps outside brain cells, and the formation of so-called fibrillary tangles by tau protein inside cells — have both been well investigated in Alzheimer’s disease. Tau proteins are necessary components of healthy brain nerve cells, but in Alzheimer’s, unknown factors increase the labels — in the form of phosphate molecules — normally
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