Abstract
Free radical production is central to the development and pathogenesis of central nervous system (CNS) inflammation, the vascular and cellular response that results in the accumulation of circulating cells and factors in CNS tissues. Oxygen- and nitrogen-based radicals produced by invading neutrophils and monocytes have been implicated in the CNS tissue damage that occurs in multiple sclerosis, viral encephalitis, and other neuroinflammatory diseases, secondary inflammation following CNS injury, and a number of neurodegenerative conditions with inflammatory elements, such as Parkinson’s and Alzheimer’s diseases. However in addition to cytotoxic effects, there is accumulating evidence that radical activity contributes to the increased blood–brain barrier (BBB) permeability associated with the invasion of leukocytes into the tissues in both pathological and protective CNS immune responses. Radical production during different types of CNS inflammatory conditions is reviewed from the perspective that the sources and nature of the radicals produced at least partly dictate the extent of CNS tissue pathology. Therapeutic strategies to control the production or activity of free radicals in the CNS are also discussed.
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