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Axonal protection using flecainide in experimental autoimmune encephalomyelitis
Author(s) -
Bechtold David A.,
Kapoor Raju,
Smith Kenneth J.
Publication year - 2004
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20045
Subject(s) - flecainide , experimental autoimmune encephalomyelitis , neuroscience , medicine , multiple sclerosis , encephalomyelitis , immunology , biology , atrial fibrillation
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.