The relation of oxidative stress and hyperexcitation to neurological disease.
The expression of a considerable range of neurological diseases is thought to involve two pathological states, namely, the production of excessive amounts of reactive oxygen species and neuronal hyperactivity. These events may represent an outcome of general vulnerable features of nervous tissue. Since they are associated with many unrelated diseases, the phenomena may be considered the final common pathways of a range of metabolic defects. Superimposed on these general signs of cellular impairment are the more specific features of each disorder. This review describes some of the evidence for the presence of hyperactivity and oxidative stress in various neurological disorders. Mechanisms whereby the states may interact and modulate each other are discussed. The manner in which such understanding has implications for the development of novel therapeutic approaches is also described.
Bondy
S C
SC
Department of Community and Environmental Medicine, University of California, Irvine 92717-1825.
D000544:Alzheimer Disease / Q000503:physiopathology; D000690:Amyotrophic Lateral Sclerosis / Q000503:physiopathology; D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000503:physiopathology; D004827:Epilepsy / Q000503:physiopathology; D006801:Humans; D006816:Huntington Disease / Q000503:physiopathology; D008659:Metabolic Diseases / Q000503:physiopathology; D009422:Nervous System Diseases / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000503:physiopathology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012640:Seizures / Q000503:physiopathology
D017382:Reactive Oxygen Species