Multiple sclerosis (MS) is a neurodegenerative disease that is deemed to affect more than 2.1 million people worldwide, and for which there is no cure. Early symptoms of MS are believed to result from axonal demyelination leading to slowing or blockade of impulse conduction. The blockade of K+ channels has been proven to improve conduction deficiencies secondary to demyelination in patients with MS. Dalfampridine is a K+ channel blocker that was recently approved by FDA for the symptomatic treatment of ambulation hardship in MS. Understanding the mechanisms by which Dalfampridine exerts its therapeutic effects is a complex issue as it blocks a wide variety of K+ channels that are distributed across multiple cell types in the nervous system but also in the immune system, and because of their molecular identities remaining unknown. This review describes Dalfampridine potential roles at the cellular and molecular levels in MS pathogenesis.
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