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NEUROLOGY 2004;63:S3-S7
© 2004 American Academy of Neurology

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

Immunopathology of multiple sclerosis

Edward J. Fox, MD, PhD

From the Multiple Sclerosis Clinic of Central Texas, Round Rock, Texas.

Address correspondence and reprint requests to Dr. Edward J. Fox, Multiple Sclerosis Clinic of Central Texas, 7200 Wyoming Springs Dr., Suite 1100, Round Rock, TX 78681; e-mail: FoxTex{at}aol.com

Multiple sclerosis (MS) is an immune-mediated disease of the CNS that is characterized by inflammation, demyelination, and axon loss. The inflammation in MS appears to be caused by an overactive pro-inflammatory TH1 profile in T cells. Demyelination can result as a consequence of direct damage to myelin by inflammatory cells or indirectly because of the environment produced by inflammation. Axon loss occurs in MS lesions starting early in the disease. Treatments now approved by the FDA are most effective in the inflammatory phase of the disease. Because axon loss is irreversible and is responsible for long-term disability, therapies are also needed that enhance remyelination or are neuroprotective.




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