摘要
Tau protein (encoded by the MAPT gene) is an attractive therapeutic target for the treatment of Alzheimer’s disease (AD) and other “tauopathies”, where aggregated tau pathology accumulates in neurons. Since tau deposition is strongly associated with cognitive dysfunction in AD, and tau purportedly mediates the toxicity of β-amyloid, therapies developed to reduce tau or its phosphorylation have been tested preclinically and in several small-scale clinical trials[1]. However, caveats for tau-targeting therapy include the limited understanding of its physiological functions and the complicated interactions between its post-translational modifications, aggregation, and cellular toxicity.
作者
雷鹏
Scott Ayton
Peng Lei;Scott Ayton(Department of Neurology and State Key Laboratory of Biotherapy,National Clinical Research Center for Geriatrics,West China Hospital,Sichuan University,Chengdu 610041,China;The Florey Neuroscience Institute,The University of Melbourne,Melbourne VIC 3052,Australia)
基金
supported by the National Clinical Research Center for Geriatrics of West China Hospital (Z2021LC001)
the West China Hospital 1.3.5 Project for Disciplines of Excellence(ZYYC20009)。