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• W2529470828 abstract "Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins. As growing evidence indicates that reducing the steady-state levels of disease-causing proteins mitigates neurodegeneration in animal models, we developed a strategy to screen for genes that decrease the levels of tau, whose accumulation contributes to the pathology of both Alzheimer disease (AD) and progressive supranuclear palsy (PSP). Integrating parallel cell-based and Drosophila genetic screens, we discovered that tau levels are regulated by Nuak1, an AMPK-related kinase. Nuak1 stabilizes tau by phosphorylation specifically at Ser356. Inhibition of Nuak1 in fruit flies suppressed neurodegeneration in tau-expressing Drosophila, and Nuak1 haploinsufficiency rescued the phenotypes of a tauopathy mouse model. These results demonstrate that decreasing total tau levels is a valid strategy for mitigating tau-related neurodegeneration and reveal Nuak1 to be a novel therapeutic entry point for tauopathies." @default.
• W2529470828 created "2016-10-14" @default.
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• W2529470828 date "2016-10-01" @default.
• W2529470828 modified "2023-10-17" @default.
• W2529470828 title "Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model" @default.
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• W2529470828 doi "https://doi.org/10.1016/j.neuron.2016.09.022" @default.
• W2529470828 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5745060" @default.
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