Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis

Manuel A Friese; Benjamin Schattling; Lars Fugger

doi:10.1038/nrneurol.2014.37

Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis

Standard

Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. / Friese, Manuel A ; Schattling, Benjamin; Fugger, Lars.

In: NAT REV NEUROL, Vol. 10, No. 4, 2014, p. 225-38.

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

Harvard

Friese, MA , Schattling, B & Fugger, L 2014, 'Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis', NAT REV NEUROL, vol. 10, no. 4, pp. 225-38. https://doi.org/10.1038/nrneurol.2014.37

APA

Friese, M. A., Schattling, B., & Fugger, L. (2014). Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. NAT REV NEUROL, 10(4), 225-38. https://doi.org/10.1038/nrneurol.2014.37

Vancouver

Friese MA , Schattling B, Fugger L. Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. NAT REV NEUROL. 2014;10(4):225-38. https://doi.org/10.1038/nrneurol.2014.37

Bibtex

@article{1653d220a4b0409796af57f3d74e25f7,

title = "Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis",

abstract = "Multiple sclerosis (MS) is the most frequent chronic inflammatory disease of the CNS, and imposes major burdens on young lives. Great progress has been made in understanding and moderating the acute inflammatory components of MS, but the pathophysiological mechanisms of the concomitant neurodegeneration--which causes irreversible disability--are still not understood. Chronic inflammatory processes that continuously disturb neuroaxonal homeostasis drive neurodegeneration, so the clinical outcome probably depends on the balance of stressor load (inflammation) and any remaining capacity for neuronal self-protection. Hence, suitable drugs that promote the latter state are sorely needed. With the aim of identifying potential novel therapeutic targets in MS, we review research on the pathological mechanisms of neuroaxonal dysfunction and injury, such as altered ion channel activity, and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction. We focus on mechanisms inherent to neurons and their axons, which are separable from those acting on inflammatory responses and might, therefore, represent bona fide neuroprotective drug targets with the capability to halt MS progression.",

author = "Friese, {Manuel A} and Benjamin Schattling and Lars Fugger",

year = "2014",

doi = "10.1038/nrneurol.2014.37",

language = "English",

volume = "10",

pages = "225--38",

journal = "NAT REV NEUROL",

issn = "1759-4758",

publisher = "NATURE PUBLISHING GROUP",

number = "4",

}

RIS

TY - JOUR

T1 - Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis

AU - Friese, Manuel A

AU - Schattling, Benjamin

AU - Fugger, Lars

PY - 2014

Y1 - 2014

N2 - Multiple sclerosis (MS) is the most frequent chronic inflammatory disease of the CNS, and imposes major burdens on young lives. Great progress has been made in understanding and moderating the acute inflammatory components of MS, but the pathophysiological mechanisms of the concomitant neurodegeneration--which causes irreversible disability--are still not understood. Chronic inflammatory processes that continuously disturb neuroaxonal homeostasis drive neurodegeneration, so the clinical outcome probably depends on the balance of stressor load (inflammation) and any remaining capacity for neuronal self-protection. Hence, suitable drugs that promote the latter state are sorely needed. With the aim of identifying potential novel therapeutic targets in MS, we review research on the pathological mechanisms of neuroaxonal dysfunction and injury, such as altered ion channel activity, and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction. We focus on mechanisms inherent to neurons and their axons, which are separable from those acting on inflammatory responses and might, therefore, represent bona fide neuroprotective drug targets with the capability to halt MS progression.

AB - Multiple sclerosis (MS) is the most frequent chronic inflammatory disease of the CNS, and imposes major burdens on young lives. Great progress has been made in understanding and moderating the acute inflammatory components of MS, but the pathophysiological mechanisms of the concomitant neurodegeneration--which causes irreversible disability--are still not understood. Chronic inflammatory processes that continuously disturb neuroaxonal homeostasis drive neurodegeneration, so the clinical outcome probably depends on the balance of stressor load (inflammation) and any remaining capacity for neuronal self-protection. Hence, suitable drugs that promote the latter state are sorely needed. With the aim of identifying potential novel therapeutic targets in MS, we review research on the pathological mechanisms of neuroaxonal dysfunction and injury, such as altered ion channel activity, and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction. We focus on mechanisms inherent to neurons and their axons, which are separable from those acting on inflammatory responses and might, therefore, represent bona fide neuroprotective drug targets with the capability to halt MS progression.

U2 - 10.1038/nrneurol.2014.37

DO - 10.1038/nrneurol.2014.37

M3 - SCORING: Journal article

C2 - 24638138

VL - 10

SP - 225

EP - 238

JO - NAT REV NEUROL

JF - NAT REV NEUROL

SN - 1759-4758

IS - 4

ER -