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Original Articles
Axonal protection using flecainide in experimental autoimmune encephalomyelitis
Article first published online: 21 MAR 2004
DOI: 10.1002/ana.20045
Copyright © 2003 American Neurological Association
1531-8249/asset/cover.gif?v=1&s=685ec69724c5ed4c8847ce939e70ceb45065856f "Annals of Neurology")
Additional Information
How to Cite
Bechtold, D. A., Kapoor, R. and Smith, K. J. (2004), Axonal protection using flecainide in experimental autoimmune encephalomyelitis. Ann Neurol., 55: 607–616. doi: 10.1002/ana.20045
Publication History
- Issue published online: 21 APR 2004
- Article first published online: 21 MAR 2004
- Manuscript Revised: 22 DEC 2003
- Manuscript Accepted: 22 DEC 2003
- Manuscript Received: 2 SEP 2003
Funded by
- Multiple Sclerosis Society of Great Britain and Northern Ireland
- Abstract
- Article
- References
- Cited By
Abstract
Axonal degeneration is a major cause of permanent neurological deficit in multiple sclerosis (MS), but no current therapies for the disease are known to be effective at axonal protection. Here, we examine the ability of a sodium channel–blocking agent, flecainide, to reduce axonal degeneration in an experimental model of MS, chronic relapsing experimental autoimmune encephalomyelitis (CR-EAE). Rats with CR-EAE were treated with flecainide or vehicle from either 3 days before or 7 days after inoculation (dpi) until termination of the experiment at 28 to 30 dpi. Morphometric examination of neurofilament-labeled axons in the spinal cord of CR-EAE animals showed that both flecainide treatment regimens resulted in significantly higher numbers of axons surviving the disease (83 and 98% of normal) compared with controls (62% of normal). These findings indicate that flecainide and similar agents may provide a novel therapy aimed at axonal protection in MS and other neuroinflammatory disorders.