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- W2012666269 abstract "Pathologic alterations in the microtubule-associated protein tau have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal dementia (FTD). Here, we show that tau overexpression, in combination with phosphorylation by the Drosophila glycogen synthase kinase-3 (GSK-3) homolog and wingless pathway component (Shaggy), exacerbated neurodegeneration induced by tau overexpression alone, leading to neurofibrillary pathology in the fly. Furthermore, manipulation of other wingless signaling molecules downstream from shaggy demonstrated that components of the Wnt signaling pathway modulate neurodegeneration induced by tau pathology in vivo but suggested that tau phosphorylation by GSK-3β differs from canonical Wnt effects on β-catenin stability and TCF activity. The genetic system we have established provides a powerful reagent for identification of novel modifiers of tau-induced neurodegeneration that may serve as future therapeutic targets." @default.
- W2012666269 created "2016-06-24" @default.
- W2012666269 creator A5018481303 @default.
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- W2012666269 creator A5055815966 @default.
- W2012666269 creator A5082234952 @default.
- W2012666269 creator A5087559967 @default.
- W2012666269 date "2002-05-01" @default.
- W2012666269 modified "2023-10-18" @default.
- W2012666269 title "Human Wild-Type Tau Interacts with wingless Pathway Components and Produces Neurofibrillary Pathology in Drosophila" @default.
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