期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 20, 期 -, 页码 S357-S367出版社
IOS PRESS
DOI: 10.3233/JAD-2010-100498
关键词
Apoptosis; autophagy; mitochondria; neurodegeneration; reactive oxygen species
资金
- Canadian Institutes of Health Research (CIHR)
- Parkinson's Research Consortium
- Parkinson's Society of Canada
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.
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