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Acquired channelopathies as contributors to development and progression of multiple sclerosis.

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Affiliations

  • 1. Zentrum für Molekulare Neurobiologie, Universitätsklinikum Hamburg-Eppendorf, Falkenried 94, D-20251 Hamburg, Germany.
      Authors
    • Schattling B 1
    • Eggert B 1
    • Friese MA 1
    (3 authors)

ORCIDs linked to this article

Experimental Neurology, 20 Mar 2014, 262 Pt A:28-36
https://doi.org/10.1016/j.expneurol.2013.12.006 PMID: 24656770 

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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.

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Read article at publisher's site: https://doi.org/10.1016/j.expneurol.2013.12.006

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Funding 

Funders who supported this work.

Boehringer Ingelheim Stiftung Exploration Grant

    Deutsche Forschungsgemeinschaft Emmy Noether-Programme (1)

    Forschung- und Wissenschaftsstiftung Hamburg

      Gemeinnützige Hertie-Stiftung (2)

      Werner Otto Stiftung