The Association of Tau With Mitochondrial Dysfunction in Alzheimer's Disease

被引:164
|
作者
Cheng, Ying [1 ]
Bai, Feng [2 ]
机构
[1] Southeast Univ, Sch Med, Affiliated ZhongDa Hosp, Dept Neurol, Nanjing, Jiangsu, Peoples R China
[2] Nanjing Univ, Med Sch, Drum Tower Hosp, Dept Neurol, Nanjing, Jiangsu, Peoples R China
来源
FRONTIERS IN NEUROSCIENCE | 2018年 / 12卷
基金
中国国家自然科学基金;
关键词
Alzheimer's disease; tau; mitochondrial transport; mitochondrial dynamics; mitochondrial dysfunction; AXONAL-TRANSPORT DEFECTS; OXIDATIVE STRESS; PHOSPHORYLATED TAU; AMYLOID-BETA; NEURODEGENERATIVE DISEASES; HYPERPHOSPHORYLATED TAU; SYNAPTIC DYSFUNCTION; ABNORMAL INTERACTION; MOUSE MODEL; PROTEIN-TAU;
D O I
10.3389/fnins.2018.00163
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Increasing evidence suggests that abnormally hyperphosphorylated tau plays a vital role in the pathogenesis of Alzheimer's disease (AD). Mitochondrial dysfunction also has a recognized role in the pathophysiology of AD. In recent years, mitochondrial dysfunction has been strongly associated with tau pathology in AD. Overexpression of hyperphosphorylated and aggregated tau appears to damage the axonal transport, leading to abnormal mitochondrial distribution. In addition, pathological tau impairs mitochondrial dynamics by regulating mitochondrial fission/fusion proteins, and further causes mitochondrial dysfunction and neuronal damage. Moreover, mitochondrial dysfunction is also involved in promoting tau pathology in AD. In this article, we evaluate the relationship between phosphorylated tau and mitochondrial dysfunction in AD.
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收藏
页数:6
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