Axonal conduction and injury in multiple sclerosis: the role of sodium channels.
Multiple sclerosis (MS) is the most common cause of neurological disability in young adults. Recent studies have implicated specific sodium channel isoforms as having an important role in several aspects of the pathophysiology of MS, including the restoration of impulse conduction after demyelination, axonal degeneration and the mistuning of Purkinje neurons that leads to cerebellar dysfunction. By manipulating the activity of these channels or their expression, it might be possible to develop new therapeutic approaches that will prevent or limit disability in MS.
Waxman
Stephen G
SG
Department of Neurology and Center for Neuroscience and Regeneration Research, Yale School of Medicine, New Haven, Connecticut 06510, USA. stephen.waxman@yale.edu
D000200:Action Potentials; D000818:Animals; D001369:Axons / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000503:physiopathology*; D009186:Myelin Sheath / Q000378:metabolism; D062557:NAV1.6 Voltage-Gated Sodium Channel; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000473:pathology; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000378:metabolism; D009431:Neural Conduction; D015222:Sodium Channels / Q000235:genetics / Q000378:metabolism*; D014855:Wallerian Degeneration / Q000378:metabolism* / Q000503:physiopathology*
D062557:NAV1.6 Voltage-Gated Sodium Channel; D009419:Nerve Tissue Proteins; C100681:SCN8A protein, human; D015222:Sodium Channels