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Reactive Oxygen Species: Stuck in the Middle of Neurodegeneration

Issue title: Mitochondria and Neurodegenerative Diseases

Guest editors: Xiongwei Zhu, M. Flint Beal, Xinglong Wang, George Perry and Mark A. Smith

Article type: Review Article

Authors: Patten, David A.; | Germain, Marc; | Kelly, Melissa A. | Slack, Ruth S.; *

Affiliations: Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON, Canada

Correspondence: [*] Correspondence to: Ruth S. Slack, Ph.D., Ottawa Health Research Institute, University of Ottawa, 451 Smyth Road, Ottawa, ON, Canada K1H 8M5. Tel.: +1 613 562 5800, ext. 8458; Fax: +1 613 562 5403; E-mail: rslack@uottawa.ca.

Note: [1] These authors contributed equally to this work.

Keywords: Apoptosis, autophagy, mitochondria, neurodegeneration, reactive oxygen species

DOI: 10.3233/JAD-2010-100498

Journal: Journal of Alzheimer's Disease, vol. 20, no. s2, pp. S357-S367, 2010

Accepted 5 April 2010
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Published: 3 June 2010
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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.

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