The pathophysiology of reactive oxygen intermediates in the central nervous system.
Current evidence for the participation of free radicals in diseases of the central nervous system is reviewed. We conclude that the pathogenesis is based on a uniform mechanism: free radicals preferentially attack myelin, which contains easily peroxidizable phospholipids. The basal ganglia seem to be a brain area that is especially susceptible to radical damage which is possibly related to the synthesis of neurotransmitters. The clinical picture of the resulting cell death is dominated by convulsions and retardation in childhood and by psychomotoric disability and dementia in adulthood.
Weber
G F
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Dana-Farber Cancer Institute, Boston, MA 02115.
D016923:Cell Death; D002493:Central Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D003704:Dementia / Q000209:etiology; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D008607:Intellectual Disability / Q000209:etiology; D009186:Myelin Sheath / Q000378:metabolism; D011596:Psychomotor Disorders / Q000209:etiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012640:Seizures / Q000209:etiology
D005609:Free Radicals; D017382:Reactive Oxygen Species