活性氧簇：在神经退行性病变中陷入困境。

Reactive oxygen species: stuck in the middle of neurodegeneration.

机构信息

Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada.

出版信息

J Alzheimers Dis. 2010;20 Suppl 2:S357-67. doi: 10.3233/JAD-2010-100498.

DOI:10.3233/JAD-2010-100498

PMID:20421690

Abstract

Neuronal cell loss associated with neurodegeneration has recently been linked to mitochondrial dysfunction. Electron transport chain defects and reactive oxygen species (ROS) production are emerging as important players in the etiology of neurodegenerative diseases. Proper management of ROS and disposal of damaged cellular components are vital to the survival and function of neurons. Proteins involved in these pathways are often mutated in neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. In this review, we will discuss the roles of ROS in normal physiology, how changes in ROS production affect neuronal survival in neurodegenerative diseases, and the recent advances in mitochondrial antioxidants as potential therapeutics.

摘要

神经元细胞的丢失与神经退行性变有关，最近与线粒体功能障碍有关。电子传递链缺陷和活性氧（ROS）的产生正成为神经退行性疾病病因学中的重要因素。ROS 的适当管理和受损细胞成分的处理对于神经元的存活和功能至关重要。这些途径中涉及的蛋白质在神经退行性疾病（如阿尔茨海默病、帕金森病、肌萎缩侧索硬化症和亨廷顿病）中经常发生突变。在这篇综述中，我们将讨论 ROS 在正常生理中的作用，ROS 产生的变化如何影响神经退行性疾病中神经元的存活，以及线粒体抗氧化剂作为潜在治疗方法的最新进展。