Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Action Potentials
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Animals
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Axons / metabolism*
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Axons / pathology
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Humans
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Multiple Sclerosis / metabolism*
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Multiple Sclerosis / physiopathology*
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Myelin Sheath / metabolism
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NAV1.6 Voltage-Gated Sodium Channel
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Nerve Fibers, Myelinated / metabolism
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Nerve Fibers, Myelinated / pathology
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Nerve Tissue Proteins / genetics
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Nerve Tissue Proteins / metabolism
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Neural Conduction
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Sodium Channels / genetics
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Sodium Channels / metabolism*
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Wallerian Degeneration / metabolism*
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Wallerian Degeneration / physiopathology*
Substances
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NAV1.6 Voltage-Gated Sodium Channel
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Nerve Tissue Proteins
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SCN8A protein, human
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Sodium Channels