Oxidative stress in neurodegenerative diseases

• Published in: Annual review of pharmacology and toxicology Vol. 36; pp. 83 - 106
• Main Authors: Simonian, N A, Coyle, J T
• Format: Journal Article
• Language: English
• Published: United States Annual Reviews, Inc 1996
• Subjects: Alzheimer Disease - physiopathology; Amyotrophic Lateral Sclerosis - physiopathology; Apoptosis - physiology; Arachidonic Acid - metabolism; Electron Transport; Endopeptidases - metabolism; Enzyme Activation; Free Radicals - adverse effects; Free Radicals - metabolism; Humans; Mitochondria - metabolism; Necrosis - physiopathology; Nerve Degeneration - physiology; Nitric Oxide - metabolism; Oxidation-Reduction; Oxidative Stress; Parkinson Disease - physiopathology
• ISBN: 0824304365; 9780824304362
• ISSN: 0362-1642; 1545-4304
• DOI: 10.1146/annurev.pa.36.040196.000503

Oxidative stress refers to the cytopathologic consequences of a mismatch between the production of free radicals and the ability of the cell to defend against them. Growing data from experimental models and human brain studies suggest oxidative stress may play an important role in neuronal degeneration in diseases such as Parkinson's disease, Alzheimer's disease, and amyotrophic lateral sclerosis. Mitochondrial oxidative metabolism, nitric oxide, phospholipid metabolism, and proteolytic pathways are potential sources of intracellular free radicals. Alterations in free radical defense systems may also contribute to oxidative stress. A net increase in reactive oxygen species can produce damage to lipids, proteins, and DNA and induce necrosis or apoptosis. Elucidating the pathways important in the production of and defense from free radicals may be important in devising new pharmacologic strategies to slow or halt neuronal degeneration.