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dc.rights.licenseopenen_US
dc.contributor.authorTREMBLAY, Marie-Eve
hal.structure.identifierNutrition et Neurobiologie intégrée [NutriNeuro]
dc.contributor.authorMADORE, Charlotte
dc.contributor.authorBORDELEAU, Maude
dc.contributor.authorTIAN, Li
dc.contributor.authorVERKHRATSKY, Alexei
dc.date.accessioned2023-05-24T09:41:02Z
dc.date.available2023-05-24T09:41:02Z
dc.date.issued2020-11-11
dc.identifier.issn1662-5102en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/182295
dc.description.abstractEnSARS-CoV-2, which causes the Coronavirus Disease 2019 (COVID-19) pandemic, has a brain neurotropism through binding to the receptor angiotensin-converting enzyme 2 expressed by neurones and glial cells, including astrocytes and microglia. Systemic infection which accompanies severe cases of COVID-19 also triggers substantial increase in circulating levels of chemokines and interleukins that compromise the blood-brain barrier, enter the brain parenchyma and affect its defensive systems, astrocytes and microglia. Brain areas devoid of a blood-brain barrier such as the circumventricular organs are particularly vulnerable to circulating inflammatory mediators. The performance of astrocytes and microglia, as well as of immune cells required for brain health, is considered critical in defining the neurological damage and neurological outcome of COVID-19. In this review, we discuss the neurotropism of SARS-CoV-2, the implication of neuroinflammation, adaptive and innate immunity, autoimmunity, as well as astrocytic and microglial immune and homeostatic functions in the neurological and psychiatric aspects of COVID-19. The consequences of SARS-CoV-2 infection during ageing, in the presence of systemic comorbidities, and for the exposed pregnant mother and foetus are also covered.
dc.language.isoENen_US
dc.rights.urihttp://creativecommons.org/licenses/by/
dc.subject.enCOVID-19
dc.subject.enSARS-CoV-2
dc.subject.enimmunity
dc.subject.enastrocyte
dc.subject.enmicroglia
dc.subject.enageing
dc.subject.encomorbidity
dc.subject.endevelopment
dc.title.enNeuropathobiology of COVID-19: the role for glia
dc.typeArticle de revueen_US
dc.identifier.doi10.3389/fncel.2020.592214en_US
dc.subject.halSciences du Vivant [q-bio]en_US
dc.identifier.pubmed33304243en_US
bordeaux.journalFrontiers in Cellular Neuroscienceen_US
bordeaux.page1-15en_US
bordeaux.volume14en_US
bordeaux.hal.laboratoriesNutriNeuro (Laboratoire de Nutrition et Neurobiologie Intégrée) - UMR 1286en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINRAEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcehal
hal.identifierhal-03172929
hal.version1
hal.exportfalse
workflow.import.sourcehal
dc.rights.ccPas de Licence CCen_US
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