Abstract
The aetiology of multiple sclerosis suggests that its occurrence depends on a combination of factors, including viral infection in early childhood, genotype and an initiating event within the central nervous system. The resulting damage may be caused by events initiated by free radicals. Free radicals themselves may cause damage to myelin and also may trigger the arachidonic acid cascade, to produce compounds that are thought to initiate and augment T-cell activity. Repair of the damaged tissue is normally achieved by protective enzymes that remove damaged lipid from the myelin.
MeSH terms
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Antigens, Surface / biosynthesis*
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Cell Adhesion Molecules / metabolism
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Free Radicals
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Humans
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Interferons / physiology
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Lipid Peroxides / metabolism*
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Models, Neurological*
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Multiple Sclerosis / etiology*
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Multiple Sclerosis / immunology
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Optic Neuritis / metabolism
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Optic Neuritis / pathology
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Oxidative Stress
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Phospholipases A / metabolism
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Superoxide Dismutase / metabolism
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T-Lymphocytes / immunology
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Tumor Necrosis Factor-alpha / physiology
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Virus Diseases / complications*
Substances
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Antigens, Surface
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Cell Adhesion Molecules
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Free Radicals
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Lipid Peroxides
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Tumor Necrosis Factor-alpha
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Interferons
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Superoxide Dismutase
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Phospholipases A