Sodium-mediated axonal degeneration in inflammatory demyelinating disease

David A. Bechtold, Kenneth J. Smith

    Research output: Contribution to journalArticlepeer-review


    Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS). The mechanisms responsible for the degeneration remain unclear, but evidence suggests that a failure to maintain axonal sodium ion homeostasis may be a key step that underlies at least some of the degeneration. Sodium ions can accumulate within axons due to a series of events, including impulse activity and exposure to inflammatory factors such as nitric oxide. Recent findings have demonstrated that partial blockade of sodium channels can protect axons from nitric oxide-mediated degeneration in vitro, and from the effects of neuroinflammatory disease in vivo. This review describes some of the reasons why sodium ions might be expected to accumulate within axons in MS, and recent observations suggesting that it is possible to protect axons from degeneration in neuroinflammatory disease by partial sodium channel blockade. © 2005 Elsevier B.V. All rights reserved.
    Original languageEnglish
    Pages (from-to)27-35
    Number of pages8
    Issue number1-2
    Publication statusPublished - 15 Jun 2005


    • Demyelination
    • Energy depletion
    • Experimental autoimmune encephalomyelitis (EAE)
    • Hypoxia
    • Nitric oxide
    • Sodium channel


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