Acquired channelopathies as contributors to development and progression of multiple sclerosis
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Acquired channelopathies as contributors to development and progression of multiple sclerosis. / Schattling, Benjamin; Eggert, Britta; Friese, Manuel A.
in: EXP NEUROL, Jahrgang 262 Pt A, 01.12.2014, S. 28-36.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Acquired channelopathies as contributors to development and progression of multiple sclerosis
AU - Schattling, Benjamin
AU - Eggert, Britta
AU - Friese, Manuel A
N1 - Copyright © 2013 Elsevier Inc. All rights reserved.
PY - 2014/12/1
Y1 - 2014/12/1
N2 - 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.
AB - 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.
KW - Animals
KW - Central Nervous System
KW - Channelopathies
KW - Disease Progression
KW - Humans
KW - Multiple Sclerosis
U2 - 10.1016/j.expneurol.2013.12.006
DO - 10.1016/j.expneurol.2013.12.006
M3 - SCORING: Journal article
C2 - 24656770
VL - 262 Pt A
SP - 28
EP - 36
JO - EXP NEUROL
JF - EXP NEUROL
SN - 0014-4886
ER -