Oxidative stress, mitochondrial damage and neurodegenerative diseases

Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which ca...

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Published in:	Neural regeneration research Vol. 8; no. 21; pp. 2003 - 2014
Main Authors:	Guo, Chunyan, Sun, Li, Chen, Xueping, Zhang, Danshen
Format:	Journal Article
Language:	English
Published:	India Medknow Publications and Media Pvt. Ltd 25-07-2013 Medknow Publications & Media Pvt. Ltd Department of Pharmacy, Hebei North University, Zhangjiakou 075000, Hebei Province, China%Life Science Research Center, Hebei North University, Zhangjiakou 075000, Hebei Province, China%Department of Human Anatomy and Cell Science, University of Manitoba, Manitoba R3E 0J9, Canada%Hebei University of Science and Technology, Shijiazhuang 050018, Hebei Province, China Medknow Publications & Media Pvt Ltd
Subjects:	Adenosine triphosphate Amyotrophic lateral sclerosis Cytochrome Degeneration Dehydrogenases Deoxyribonucleic acid DNA DNA damage Enzymes Free radicals Gene expression Homeostasis Lipids Metabolism Mitochondria Mitochondrial DNA Mutation Nervous system Neurodegeneration Oxidation Oxidative stress Parkinson's disease Permeability Phosphorylation Physiological aspects Physiology Proteins Review Sulfur 功能障碍发病机制损伤氧化应激神经变性疾病神经退行性疾病线粒体DNA突变阿尔茨海默病 neurodegenerative diseases Parkinson's disease neural regeneration neuroregeneration grants-supported paper reactive oxygen species mitochondrial damage Alzheimer's disease amyotrophic lateral sclerosis oxidative stress respiratory chain Alzheimer’s disease Parkinson’s disease
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Summary:	Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2＋ homeostasis and mitochondrial defense systems. All these changes are implicated in the development of these neurodegenerative diseases, mediating or amplifying neuronal dysfunction and triggering neurodegeneration. This paper summarizes the contribution of oxidative stress and mitochondrial damage to the onset of neurodegenerative diseases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases.
Bibliography:	neural regeneration; neurodegenerative diseases; Alzheimer’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; oxidative stress; reactive oxygen species; mitochondrial damage; respiratory chain; grants-supported paper; neuroregeneration Oxidative stress and mitochondrial damage have been implicated in the pathogenesis of several neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease and amyotrophic lateral sclerosis. Oxidative stress is characterized by the overproduction of reactive oxygen species, which can induce mitochondrial DNA mutations, damage the mitochondrial respiratory chain, alter membrane permeability, and influence Ca2＋ homeostasis and mitochondrial defense systems. All these changes are implicated in the development of these neurodegenerative diseases, mediating or amplifying neuronal dysfunction and triggering neurodegeneration. This paper summarizes the contribution of oxidative stress and mitochondrial damage to the onset of neurodegenerative diseases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases. 11-5422/R ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 Author statements: The manuscript is original, has not been submitted to or is not under consideration by another publication, has not been previously published in any language or any form, including electronic, and contains no disclosure of confidential information or authorship/patent application/funding source disputations. Chunyan Guo, Master, Professor. Author contributions: Guo CY collected and analyzed the references, conceived and designed the study, and wrote the manuscript. Sun L retrieved the references. Chen XP retrieved the references and revised the manuscript. Zhang DS was responsible for conception and design. All authors approved the final version of the paper. Chunyan Guo and Xueping Chen contributed equally to this work.
ISSN:	1673-5374 1876-7958
DOI:	10.3969/j.issn.1673-5374.2013.21.009