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Amyotrophic lateral sclerosis: The complement and inflammatory hypothesis

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@article{0929a1fd8ecc434eb0cdf33d9815c6c7,
title = "Amyotrophic lateral sclerosis: The complement and inflammatory hypothesis",
abstract = "Amyotrophic lateral sclerosis (ALS) is a devastating, neurodegenerative motor neuron disease. The aetiology of ALS remains an enigma which hinders the design of an effective treatment to prevent, postpone, or reverse the pathophysiological changes occurring during the aggressive progression of this disease. During the last decade, basic research within the innate immune system, and in particular the complement system, has revealed new, important roles of the innate immune system during development, homeostasis, and ageing within as well as outside the central nervous system. Several lines of evidence indicate that aberrant activation of the complement system locally in the central nervous system as well as systemically may be involved in the pathophysiology of ALS. This exciting new knowledge could point towards the innate immune system as a potential target of medical intervention in ALS. Recently, the historic perception of ALS as a central neurodegenerative disease has been challenged due to the significant amount of evidence of a dying-back mechanism causing the selective destruction of the motor neurons, indicating that disease onset occurs outside the borders of the blood-brain-barrier. This review addresses the function of the innate immune system during ALS. We emphasize the role of the complement system and specifically suggest the involvement of ficolin-3 from the lectin pathway in the pathophysiology of ALS.",
author = "Anne-Lene Kj{\ae}ldgaard and Katrine Pilely and Olsen, {Karsten Skovgaard} and Pedersen, {Stephen W{\o}rlich} and Lauritsen, {Anne {\O}berg} and Kirsten M{\o}ller and Peter Garred",
note = "Copyright {\textcopyright} 2018 Elsevier Ltd. All rights reserved.",
year = "2018",
month = oct,
doi = "10.1016/j.molimm.2018.06.007",
language = "English",
volume = "102",
pages = "14--25",
journal = "Molecular Immunology",
issn = "0161-5890",
publisher = "Pergamon",

}

RIS

TY - JOUR

T1 - Amyotrophic lateral sclerosis

T2 - The complement and inflammatory hypothesis

AU - Kjældgaard, Anne-Lene

AU - Pilely, Katrine

AU - Olsen, Karsten Skovgaard

AU - Pedersen, Stephen Wørlich

AU - Lauritsen, Anne Øberg

AU - Møller, Kirsten

AU - Garred, Peter

N1 - Copyright © 2018 Elsevier Ltd. All rights reserved.

PY - 2018/10

Y1 - 2018/10

N2 - Amyotrophic lateral sclerosis (ALS) is a devastating, neurodegenerative motor neuron disease. The aetiology of ALS remains an enigma which hinders the design of an effective treatment to prevent, postpone, or reverse the pathophysiological changes occurring during the aggressive progression of this disease. During the last decade, basic research within the innate immune system, and in particular the complement system, has revealed new, important roles of the innate immune system during development, homeostasis, and ageing within as well as outside the central nervous system. Several lines of evidence indicate that aberrant activation of the complement system locally in the central nervous system as well as systemically may be involved in the pathophysiology of ALS. This exciting new knowledge could point towards the innate immune system as a potential target of medical intervention in ALS. Recently, the historic perception of ALS as a central neurodegenerative disease has been challenged due to the significant amount of evidence of a dying-back mechanism causing the selective destruction of the motor neurons, indicating that disease onset occurs outside the borders of the blood-brain-barrier. This review addresses the function of the innate immune system during ALS. We emphasize the role of the complement system and specifically suggest the involvement of ficolin-3 from the lectin pathway in the pathophysiology of ALS.

AB - Amyotrophic lateral sclerosis (ALS) is a devastating, neurodegenerative motor neuron disease. The aetiology of ALS remains an enigma which hinders the design of an effective treatment to prevent, postpone, or reverse the pathophysiological changes occurring during the aggressive progression of this disease. During the last decade, basic research within the innate immune system, and in particular the complement system, has revealed new, important roles of the innate immune system during development, homeostasis, and ageing within as well as outside the central nervous system. Several lines of evidence indicate that aberrant activation of the complement system locally in the central nervous system as well as systemically may be involved in the pathophysiology of ALS. This exciting new knowledge could point towards the innate immune system as a potential target of medical intervention in ALS. Recently, the historic perception of ALS as a central neurodegenerative disease has been challenged due to the significant amount of evidence of a dying-back mechanism causing the selective destruction of the motor neurons, indicating that disease onset occurs outside the borders of the blood-brain-barrier. This review addresses the function of the innate immune system during ALS. We emphasize the role of the complement system and specifically suggest the involvement of ficolin-3 from the lectin pathway in the pathophysiology of ALS.

U2 - 10.1016/j.molimm.2018.06.007

DO - 10.1016/j.molimm.2018.06.007

M3 - Journal article

C2 - 29933890

VL - 102

SP - 14

EP - 25

JO - Molecular Immunology

JF - Molecular Immunology

SN - 0161-5890

ER -

ID: 56257116