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Front. Neurosci. | doi: 10.3389/fnins.2018.00163

The association of tau with mitochondria dysfunction in Alzheimer’s disease

  • 1Department of Neurology, Southeast University, China
  • 2Department of Neurology, Medical School of Nanjing University, China

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 mitochondria 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.

Keywords: Alzheimer's disease, tau Proteins, mitochondrial transport, mitochondrial dynamics, Mitochondrial dysfunction

Received: 16 Oct 2017; Accepted: 28 Feb 2018.

Edited by:

Jesus Avila, Universidad Autonoma de Madrid, Spain

Reviewed by:

Isidre Ferrer, Universitat de Barcelona, Spain
CHENG-XIN GONG, Institute for Basic Research in Developmental Disabilities (IBR), United States  

Copyright: © 2018 Cheng and Bai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: MD. Feng Bai, Medical School of Nanjing University, Department of Neurology, Nanjing, China,