Inflammasomes; Animals; Humans; Inflammasomes/metabolism; Neurodegenerative Diseases/pathology; Neurodegenerative Diseases/physiopathology; Signal Transduction/physiology; Brain/immunology; Brain/metabolism; Brain/pathology; Brain; Neurodegenerative Diseases; Signal Transduction; Neuroscience (all); General Neuroscience
Résumé :
[en] The mammalian CNS is an intricate and fragile structure, which on one hand is open to change in order to store information, but on the other hand is vulnerable to damage from injury, pathogen invasion or neurodegeneration. During senescence and neurodegeneration, activation of the innate immune system can occur. Inflammasomes are signalling complexes that regulate cells of the immune system, which in the brain mainly includes microglial cells. In microglia, the NLRP3 (NOD-, LRR- and pyrin domain-containing 3) inflammasome becomes activated when these cells sense proteins such as misfolded or aggregated amyloid-β, α-synuclein and prion protein or superoxide dismutase, ATP and members of the complement pathway. Several other inflammasomes have been described in microglia and the other cells of the brain, including astrocytes and neurons, where their activation and subsequent caspase 1 cleavage contribute to disease development and progression.
Disciplines :
Neurologie
Auteur, co-auteur :
HENEKA, Michael ; Department of Neurodegenerative Disease and Geriatric Psychiatry, University of Bonn, Bonn, Germany. michael.heneka@ukbonn.de ; German Center for Neurodegenerative Diseases, Bonn, Germany. michael.heneka@ukbonn.de ; Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA. michael.heneka@ukbonn.de
McManus, Róisín M; Department of Neurodegenerative Disease and Geriatric Psychiatry, University of Bonn, Bonn, Germany ; German Center for Neurodegenerative Diseases, Bonn, Germany
Latz, Eicke ; German Center for Neurodegenerative Diseases, Bonn, Germany ; Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA ; Institute of Innate Immunity, University of Bonn, Bonn, Germany
Co-auteurs externes :
yes
Langue du document :
Anglais
Titre :
Inflammasome signalling in brain function and neurodegenerative disease.
M.T.H. is supported by grants from the Deutsche Forschungsgesellschaft (DFG; DFG SFBs 1089, HE). E.L. is supported by grants from the DFG (DFG SFBs 645, 670 and 1123; TRRs 83 and 57), a grant from the US National Institutes of Health (1R01HL112661) and by a European Research Council Consolidator grant (InflammAct). E.L. and M.T.H. are members of the excellence cluster ImmunoSensation funded by the DFG. M.T.H. is supported by the European Union Joint Programme– Neurodegenerative Disease (JPND) consortium InCure (funding code 01ED1505A).
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