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Nat Clin Pract Neurol. 2008 Mar;4(3):159-69. doi: 10.1038/ncpneuro0735. Epub 2008 Jan 29.

Mechanisms of disease: sodium channels and neuroprotection in multiple sclerosis-current status.

Author information

1
Department of Neurology, LCI 707, Yale Medical School, PO Box 20818, New Haven, CT 06520-8018, USA. stephen.waxman@yale.edu

Abstract

Sodium channels can provide a route for a persistent influx of sodium ions into neurons. Over the past decade, it has emerged that sustained sodium influx can, in turn, trigger calcium ion influx, which produces axonal injury in neuroinflammatory disorders such as multiple sclerosis (MS). The development of sodium channel blockers as potential neuroprotectants in MS has proceeded rapidly, and two clinical trials are currently ongoing. The route from the laboratory to the clinic includes some complex turns, however, and a third trial was recently put on hold because of new data that suggested that sodium channel blockers might have multiple, complex actions. This article reviews the development of the concept of sodium channel blockers as neuroprotectants in MS, the path from laboratory to clinic, and the current status of research in this area.

PMID:
18227822
DOI:
10.1038/ncpneuro0735
[Indexed for MEDLINE]

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