title: The Ambiguous Relationship of Oxidative Stress, Tau Hyperphosphorylation, and Autophagy Dysfunction in Alzheimer's Disease.
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.
authors.affiliation: Institute of Neuroscience, Henan Polytechnic University, Jiaozuo 454000, China ; Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Zhenzhen
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Li
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Li
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Nannan
authors.initials: N
authors.lastname: Wei
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Zhiquan
authors.initials: Z
authors.lastname: Zhao
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Huimin
authors.initials: H
authors.lastname: Liang
authors.affiliation: Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Xinying
authors.initials: X
authors.lastname: Ji
authors.affiliation: Department of Neurology, The First Affiliated Hospital, Henan University, Kaifeng 475000, China ; Institute of Neurological Disorder, Henan University, Kaifeng 475000, China.
authors.forename: Wenwu
authors.initials: W
authors.lastname: Chen
authors.affiliation: Department of Neurology, The First Affiliated Hospital, Henan University, Kaifeng 475000, China ; Institute of Neurological Disorder, Henan University, Kaifeng 475000, China.
authors.forename: Mengzhou
authors.initials: M
authors.lastname: Xue
authors.affiliation: Institute of Neuroscience, Henan Polytechnic University, Jiaozuo 454000, China ; Laboratory of Brain Function and Molecular Neurodegeneration, Institute for Brain Science Research, School of Life Sciences, Henan University, Kaifeng 475004, China.
authors.forename: Jianshe
authors.initials: J
authors.lastname: Wei
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D000975:Antioxidants / Q000378:metabolism; D001343:Autophagy; D006801:Humans; D018384:Oxidative Stress; D010766:Phosphorylation; D017382:Reactive Oxygen Species / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species; D016875:tau Proteins