Abstract

Axonal injury in multiple sclerosis has attracted considerable interest during the past few years. It has been demonstrated in association with inflammation within active lesions, but it is also present in normal-appearing white matter. Because axonal loss appears to be responsible for persistent neurological deficits in patients with multiple sclerosis, treatment strategies to prevent damage to neurites and restore function are of paramount importance in controlling the disease process. Some of the currently available immunomodulatory therapies may also reduce axonal damage, as demonstrated using improved imaging technologies, but the precise mechanisms that could protect axons during the inflammatory attack are yet to be identified. Factors that are involved in functional impairment of axonal conduction and those elements that are responsible for direct structural damage to the axon are both potential targets for therapeutic interventions.

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