The neuritic plaque facilitates pathological conversion of tau in an Alzheimer’s disease mouse model

Tong Li (), Kerstin E. Braunstein, Juhong Zhang, Ashley Lau, Leslie Sibener, Christopher Deeble and Philip C. Wong
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Tong Li: The Johns Hopkins University School of Medicine
Kerstin E. Braunstein: The Johns Hopkins University School of Medicine
Juhong Zhang: The Johns Hopkins University School of Medicine
Ashley Lau: The Johns Hopkins University School of Medicine
Leslie Sibener: The Johns Hopkins University School of Medicine
Christopher Deeble: The Johns Hopkins University School of Medicine
Philip C. Wong: The Johns Hopkins University School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract A central question in Alzheimer’s Disease (AD) is whether the neuritic plaque is necessary and sufficient for the development of tau pathology. Hyperphosphorylation of tau is found within dystrophic neurites surrounding β-amyloid deposits in AD mouse models but the pathological conversion of tau is absent. Likewise, expression of a human tau repeat domain in mice is insufficient to drive the pathological conversion of tau. Here we developed an Aβ-amyloidosis mouse model that expresses the human tau repeat domain and show that in these mice, the neuritic plaque facilitates the pathological conversion of wild-type tau. We show that this tau fragment seeds the neuritic plaque-dependent pathological conversion of wild-type tau that spreads from the cortex and hippocampus to the brain stem. These results establish that in addition to the neuritic plaque, a second determinant is required to drive the conversion of wild-type tau.

Date: 2016
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DOI: 10.1038/ncomms12082

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