Acquired channelopathies as contributors to development and progression of multiple sclerosis

Benjamin Schattling; Britta Eggert; Manuel A Friese

doi:10.1016/j.expneurol.2013.12.006

Acquired channelopathies as contributors to development and progression of multiple sclerosis

Standard

Acquired channelopathies as contributors to development and progression of multiple sclerosis. / Schattling, Benjamin; Eggert, Britta; Friese, Manuel A.

In: EXP NEUROL, Vol. 262 Pt A, 01.12.2014, p. 28-36.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Schattling, B, Eggert, B & Friese, MA 2014, 'Acquired channelopathies as contributors to development and progression of multiple sclerosis', EXP NEUROL, vol. 262 Pt A, pp. 28-36. https://doi.org/10.1016/j.expneurol.2013.12.006

APA

Schattling, B., Eggert, B., & Friese, M. A. (2014). Acquired channelopathies as contributors to development and progression of multiple sclerosis. EXP NEUROL, 262 Pt A, 28-36. https://doi.org/10.1016/j.expneurol.2013.12.006

Vancouver

Schattling B, Eggert B, Friese MA. Acquired channelopathies as contributors to development and progression of multiple sclerosis. EXP NEUROL. 2014 Dec 1;262 Pt A:28-36. https://doi.org/10.1016/j.expneurol.2013.12.006

Bibtex

@article{b4664858ee7843518a17fe89a075c93b,

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.",

keywords = "Animals, Central Nervous System, Channelopathies, Disease Progression, Humans, Multiple Sclerosis",

author = "Benjamin Schattling and Britta Eggert and Friese, {Manuel A}",

year = "2014",

month = dec,

day = "1",

doi = "10.1016/j.expneurol.2013.12.006",

language = "English",

volume = "262 Pt A",

pages = "28--36",

journal = "EXP NEUROL",

issn = "0014-4886",

publisher = "Academic Press Inc.",

}

RIS

TY - JOUR

T1 - Acquired channelopathies as contributors to development and progression of multiple sclerosis

AU - Schattling, Benjamin

AU - Eggert, Britta

AU - Friese, Manuel A

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 -