关于阿尔茨海默病中Tau蛋白导致的线粒体功能障碍的研究进展  

Research progress of mitochondrial dysfunction caused by the tau protein

作　　者：黄强[1] 李琼[1] 李清华[1] 

机构地区：[1]桂林医学院附属医院神经内科,541004

出　　处：《国际遗传学杂志》2014年第4期173-177,共5页International Journal of Genetics

基　　金：国家自然科学基金（81160163）

摘　　要：Tau蛋白是一种微管相关性蛋白，在神经变性疾病中扮演着重要角色，尤其在阿尔茨海默病（AD）中，Tau蛋白的过度磷酸化被视为特征性的病理学表现。尽管过度磷酸化Tau蛋白能够导致线粒体功能障碍进而引起了相应的临床疾病，但其导致线粒体功能障碍的具体机制尚不明确，越来越多的学者认为Tau蛋白导致线粒体功能障碍并不是通过一个单一的过程，虽然在神经变性中的作用还存在一些争议，但是对Tau蛋白导致线粒体功能障碍的探讨可能对神经变性机制的研究提供重要的线索，该文主要就AD中Tau蛋白导致线粒体功能障碍的可能机制作一简单综述。Tau is a microtubule -associated protein, and plays an important role in neurodegen- erative diseases. The hyperphosphorylationg of Tau protein is considered as a characteristic pathogenic change, especially in Alzheimer＇ s disease. Though the hyperphosphorylated Tau protein can lead to mitochondrial dysfunction followed by corresponding diseases, the mechanism of mitochondrial dysfunction caused by Tau protein is unclear. More and more researchers have attempted to confirm that the mitochondrial dysfunction caused by Tau protein is not a single process. The study of mitochondrial dysfunction caused by Tau protein may provide a better understanding on the mechanism of neurodegeneration with important clues, though the role in neurodegeneration still remain unclear. In this paper, we make a brief review about the research progress of mitochondrial dysfunction caused by tau protein in AD.

关 键 词：TAU AD 阿尔茨海默病 线粒体 

分 类 号：R749.16[医药卫生—神经病学与精神病学]