自噬调节阿尔茨海默病中Tau蛋白代谢

Autophagy Regulates Tau Protein Metabolism in Alzheimer’s Disease

摘要: 阿尔茨海默病(Alzheimer’s disease, AD)是一种以进行性认知和行为功能障碍为主要特征的中枢神经系统退行性病变，异常磷酸化的Tau蛋白积聚形成的神经纤维缠结(Neurofibrillary tangles, NFTs)被认为是其中最主要的致病因素之一。目前，临床中用于治疗AD的大多数药物只能改善疾病的基本症状，无法从根本上阻止疾病病理过程的进展。自噬作为真核细胞中物质降解的一个重要方式，在维持内环境稳态的方面发挥着至关重要的作用。自噬调节可能是AD的一种治疗策略，也可能是延缓其进展的一种方法。本文旨在探讨自噬参与阿尔茨海默病中Tau蛋白的降解，调节自噬来减少Tau蛋白的累积从而来治疗AD，可能为今后AD的治疗提供一种的新思路。

Abstract: Alzheimer’s disease is a degenerative disease of the central nervous system characterized by pro-gressive cognitive and behavioral dysfunction. The neurofibrillary tangles formed by the accumula-tion of abnormally phosphorylated tau protein are considered to be one of the most important pathogenic factors. At present, most drugs used to treat AD in clinic can only improve the basic symptoms of the disease, but can’t fundamentally stop the progress of the pathological process of the disease. Autophagy, as an important way of substance degradation in eukaryotic cells, plays a vital role in maintaining the homeostasis of internal environment. Autophagy regulation may be a therapeutic strategy for AD or a method to delay its progress. This paper aims to explore the in-volvement of autophagy in the degradation of tau in Alzheimer’s disease and regulate autophagy to reduce the accumulation of tau protein to treat AD, which may provide a new treatment idea in the future.