title: Acquired channelopathies as contributors to development and progression of multiple sclerosis.
abstract: Multiple sclerosis (MS), the most frequent inflammatory disease of the central nervous system (CNS), affects about two and a half million individuals worldwide and causes major burdens to the patients, which develop the disease usually at the age of 20 to 40. MS is likely referable to a breakdown of immune cell tolerance to CNS self-antigens resulting in focal immune cell infiltration, activation of microglia and astrocytes, demyelination and axonal and neuronal loss. Here we discuss how altered expression patterns and dysregulated functions of ion channels contribute on a molecular level to nearly all pathophysiological steps of the disease. In particular the detrimental redistribution of ion channels along axons, as well as neuronal excitotoxicity with regard to imbalanced glutamate homeostasis during chronic CNS inflammation will be discussed in detail. Together, we describe which ion channels in the immune and nervous system commend as attractive future drugable targets in MS treatment.
authors.affiliation: Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany.
authors.forename: Benjamin
authors.initials: B
authors.lastname: Schattling
authors.affiliation: Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany.
authors.forename: Britta
authors.initials: B
authors.lastname: Eggert
authors.affiliation: Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany. Electronic address: manuel.friese@zmnh.uni-hamburg.de.
authors.forename: Manuel A
authors.initials: MA
authors.lastname: Friese
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000276:immunology / Q000473:pathology*; D053447:Channelopathies / Q000150:complications*; D018450:Disease Progression; D006801:Humans; D009103:Multiple Sclerosis / Q000209:etiology*
keywords: CNS inflammation; Experimental autoimmune encephalomyelitis; Ion channels; Multiple sclerosis; Neurodegeneration