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Region Hovedstaden - en del af Københavns Universitetshospital
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Amyotrophic lateral sclerosis: The complement and inflammatory hypothesis

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Selection and characterization of camelid nanobodies towards urokinase-type plasminogen activator

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Plasma levels of mannose-binding lectin and future risk of venous thromboembolism

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Effect of hypoxia on BOLD fMRI response and total cerebral blood flow in migraine with aura patients

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Immune regulation by fibroblasts in tissue injury depends on uPARAP-mediated uptake of collectins

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

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.

OriginalsprogEngelsk
TidsskriftMolecular Immunology
Vol/bind102
Sider (fra-til)14-25
Antal sider12
ISSN0161-5890
DOI
StatusUdgivet - okt. 2018

ID: 56257116