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Oxidative Medicine and Cellular Longevity
Volume 2015, Article ID 352723, 12 pages
http://dx.doi.org/10.1155/2015/352723
Review Article

The Ambiguous Relationship of Oxidative Stress, Tau Hyperphosphorylation, and Autophagy Dysfunction in Alzheimer’s Disease

1Institute of Neuroscience, Henan Polytechnic University, Jiaozuo 454000, China
2Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China
3Department of Neurology, The First Affiliated Hospital, Henan University, Kaifeng 475000, China
4Institute of Neurological Disorder, Henan University, Kaifeng 475000, China

Received 7 October 2014; Revised 2 March 2015; Accepted 3 March 2015

Academic Editor: Eugene A. Kiyatkin

Copyright © 2015 Zhenzhen Liu et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Alzheimer’s disease (AD) is the most common form of dementia. The pathological hallmarks of AD are amyloid plaques [aggregates of amyloid-beta (Aβ)] and neurofibrillary tangles (aggregates of tau). Growing evidence suggests that tau accumulation is pathologically more relevant to the development of neurodegeneration and cognitive decline in AD patients than Aβ plaques. Oxidative stress is a prominent early event in the pathogenesis of AD and is therefore believed to contribute to tau hyperphosphorylation. Several studies have shown that the autophagic pathway in neurons is important under physiological and pathological conditions. Therefore, this pathway plays a crucial role for the degradation of endogenous soluble tau. However, the relationship between oxidative stress, tau protein hyperphosphorylation, autophagy dysregulation, and neuronal cell death in AD remains unclear. Here, we review the latest progress in AD, with a special emphasis on oxidative stress, tau hyperphosphorylation, and autophagy. We also discuss the relationship of these three factors in AD.