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Multiple sclerosis (MS) is a chronic inflammatory disease of the CNS leading to demyelination and neurodegeneration.1 During myelination, axons undergo important rearrangements of cell adhesion molecules, ion channels, and cytoskeletal proteins generating organized molecular domains, reversed during demyelination.2 Myelinated axons have a selective distribution of ion channels, which depends on the expression of scaffold and adhesion molecules.3 There is increasing evidence that ion channels in myelinated axons have a major role in the pathodynamics of MS and thus provide potential targets for axonal protection.
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