Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications

被引:432
作者
Liu, Zewen [1 ,2 ]
Zhou, Tingyang [1 ,3 ]
Ziegler, Alexander C. [4 ]
Dimitrion, Peter [4 ]
Zuo, Li [1 ,3 ]
机构
[1] Ohio State Univ, Coll Med, Wexner Med Ctr, Radiol Sci & Resp Therapy Div,Sch Hlth & Rehabil, Columbus, OH 43210 USA
[2] Wuhan Univ, Dept Anesthesiol, Affiliated Ezhou Cent Hosp, Ezhou 436000, Peoples R China
[3] Ohio State Univ, Interdisciplinary Biophys Program, Columbus, OH 43210 USA
[4] Johns Hopkins Univ, Dept Biotechnol, Baltimore, MA 21218 USA
关键词
NIGRAL DOPAMINERGIC-NEURONS; CU; ZN SUPEROXIDE-DISMUTASE; AMYLOID-BETA-PEPTIDE; HUNTINGTONS-DISEASE; MITOCHONDRIAL DYSFUNCTION; ALZHEIMERS-DISEASE; PARKINSONS-DISEASE; SPINOCEREBELLAR ATAXIA; MUTANT HUNTINGTIN; ALPHA-TOCOPHEROL;
D O I
10.1155/2017/2525967
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Increasing numbers of individuals, particularly the elderly, suffer from neurodegenerative disorders. These diseases are normally characterized by progressive loss of neuron cells and compromised motor or cognitive function. Previous studies have proposed that the overproduction of reactive oxygen species (ROS) may have complex roles in promoting the disease development. Research has shown that neuron cells are particularly vulnerable to oxidative damage due to their high polyunsaturated fatty acid content in membranes, high oxygen consumption, and weak antioxidant defense. However, the exact molecular pathogenesis of neurodegeneration related to the disturbance of redox balance remains unclear. Novel antioxidants have shown great potential in mediating disease phenotypes and could be an area of interest for further research. In this review, we provide an updated discussion on the roles of ROS in the pathological mechanisms of Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, and spinocerebellar ataxia, as well as a highlight on the antioxidant-based therapies for alleviating disease severity.
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页数:11
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