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Amyotrophic lateral sclerosis: The complement and inflammatory hypothesis

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  1. The ficolin response to LPS challenge in mice

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  2. Common and rare genetic variants of complement components in human disease

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  3. Complement activation by cholesterol crystals triggers a subsequent cytokine response

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  4. Ficolins and the lectin pathway of complement in patients with systemic lupus erythematosus

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  1. Fatal pneumococcus meningitis in a child with complement factor ficolin-3 deficiency

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  2. Continuous EEG Monitoring in a Consecutive Patient Cohort with Sepsis and Delirium

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  3. Proteomics-Based Comparative Mapping of the Secretomes of Human Brown and White Adipocytes Reveals EPDR1 as a Novel Batokine

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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.

Original languageEnglish
JournalMolecular Immunology
Volume102
Pages (from-to)14-25
Number of pages12
ISSN0161-5890
DOIs
Publication statusPublished - Oct 2018

ID: 56257116