| Literature DB >> 24656770 |
Benjamin Schattling1, Britta Eggert1, Manuel A Friese2.
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.Entities:
Keywords: CNS inflammation; Experimental autoimmune encephalomyelitis; Ion channels; Multiple sclerosis; Neurodegeneration
Mesh:
Year: 2014 PMID: 24656770 DOI: 10.1016/j.expneurol.2013.12.006
Source DB: PubMed Journal: Exp Neurol ISSN: 0014-4886 Impact factor: 5.330