Department of Pharmacy, Hebei North University, Zhangjiakou 075000, Hebei Province, China.
Life Science Research Center, Hebei North University, Zhangjiakou 075000, Hebei Province, China.
Neural Regen Res. 2013 Jul 25;8(21):2003-14. doi: 10.3969/j.issn.1673-5374.2013.21.009.
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 Ca(2+) 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 eases and discusses strategies to modify mitochondrial dysfunction that may be attractive therapeutic interventions for the treatment of various neurodegenerative diseases.
氧化应激和线粒体损伤与几种神经退行性疾病的发病机制有关，包括阿尔茨海默病、帕金森病和肌萎缩侧索硬化症。氧化应激的特征是活性氧的过度产生，这会诱导线粒体 DNA 突变、损伤线粒体呼吸链、改变膜通透性，并影响 Ca(2+) 稳态和线粒体防御系统。所有这些变化都与这些神经退行性疾病的发展有关，介导或放大神经元功能障碍并引发神经退行性变。本文总结了氧化应激和线粒体损伤对神经退行性疾病发病的贡献，并讨论了修饰线粒体功能障碍的策略，这可能是治疗各种神经退行性疾病的有吸引力的治疗干预措施。
