自噬在阿尔茨海默病发病中作用机制的研究进展

发布时间：2017-12-28 00:09

本文关键词：自噬在阿尔茨海默病发病中作用机制的研究进展　出处：《山东医药》2016年15期 　论文类型：期刊论文

【摘要】：自噬是溶酶体介导的细胞自我处理系统,是细胞降解长寿蛋白质和功能受损的细胞器进行循环利用或维持细胞稳态的过程。阿尔茨海默病(AD)作为老年性痴呆的主要原因,其神经元内β淀粉样蛋白(Aβ)的积累导致变性和神经元凋亡,随之出现老年斑、Tau蛋白过度磷酸化及代谢障碍。自噬作为清除细胞内异常蛋白、细胞器及维持细胞稳态的细胞卫士,在AD的发生发展中有重要作用。自噬参与Aβ清除,促进Aβ降解,抑制Aβ异常聚集。同时自噬能促进Tau和磷酸化Tau的降解,自噬抑制能增加Tau的细胞毒性。轴突运输障碍影响自噬功能,轴突运输缺陷导致自噬小泡堆积和神经突起的炎性改变,影响自噬体的成熟和正常功能的发挥。
[Abstract]:Autophagy is a self processing system mediated by lysosomes, a process that cells degrade long-lived proteins and impaired functional organelles, which can recycle or maintain cell homeostasis. Blzheimer's disease (AD) is the main cause of Alzheimer's disease. The accumulation of beta amyloid protein (A beta) in neurons leads to degeneration and neuronal apoptosis, which leads to the excessive phosphorylation and metabolic disorder of senile plaques and Tau protein. Autophagy, as a cell guard for removing abnormal proteins, organelles and maintaining cell homeostasis, plays an important role in the development of AD. Autophagy participates in A beta clearance, promotes the degradation of A beta, and inhibits the abnormal aggregation of A beta. Autophagy can also promote the degradation of Tau and phosphorylated Tau, and autophagy inhibition can increase the cytotoxicity of Tau. Axonal transport disorders affect autophagy. Axonal transport defects cause autophagic vacuolar accumulation and neurite inflammatory changes, which affect the maturation and normal function of autophagy.
【作者单位】：济宁市第一人民医院;
【分类号】：R749.16
【正文快照】： 阿尔茨海默病(AD)是常见的神经退行性疾病,主要病理学特征为β淀粉样蛋白(Aβ)沉积形成老年斑(SPs)、Tau蛋白过度磷酸化引发神经元纤维缠结、神经元突触功能异常及丢失[1]。自噬是长寿蛋白和胞质细胞器降解的主要细胞代谢通路,净化自身多余或受伤细胞器。目前,对于AD发病机制

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