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Pathogenesis of axonal and neuronal damage in multiple sclerosis

From the Department of Neurosciences, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio.

Address correspondence and reprint requests to Dr. Bruce D. Trapp, Department of Neuroscience, Cleveland Clinic, 9500 Euclid Avenue, NC30, Cleveland, OH 44195 trappb{at}ccf.org

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the CNS. Approximately 2 million people worldwide have MS, with females outnumbering males 2:1. Because of its high prevalence, MS is the leading cause of nontraumatic neurologic disability in young adults in the United States and Europe. Axon loss is the major cause of irreversible disability in patients with MS. Axon damage, including transection of the axon, begins early in MS and correlates with inflammatory activity. Several mechanisms lead to axon loss, including inflammatory secretions, loss of myelin-derived support, disruption of axonal ion concentrations, energy failure, and Ca²⁺ accumulation. Therapeutic interventions directed toward each of these mechanisms need to be tested for their efficacy in enhancing axon survival and, ultimately, their ability to delay progression of neurologic disability in patients with MS.

This supplement was supported by an educational grant from Teva Neuroscience. BioScience Communications contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.

Disclosure: The authors report no conflicts of interest.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represents the opinions of the authors and is not endorsed by nor does it reflect the views of the American Academy of Neurology, Editorial Board, Editor-in-Chief, or Associate Editors of Neurology.

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