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Sökning: WFRF:(Dunning Nicholas P.) > (2020-2024) > Brain injury in COV...

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FältnamnIndikatorerMetadata
00006110naa a2200817 4500
001oai:gup.ub.gu.se/320574
003SwePub
008240528s2022 | |||||||||||000 ||eng|
024a https://gup.ub.gu.se/publication/3205742 URI
024a https://doi.org/10.1093/brain/awac3212 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Needham, E. J.4 aut
2451 0a Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses
264 c 2022-09-06
264 1b Oxford University Press (OUP),c 2022
520 a COVID-19 is associated with neurological complications including stroke, delirium and encephalitis. Furthermore, a post-viral syndrome dominated by neuropsychiatric symptoms is common, and is seemingly unrelated to COVID-19 severity. The true frequency and underlying mechanisms of neurological injury are unknown, but exaggerated host inflammatory responses appear to be a key driver of COVID-19 severity. We investigated the dynamics of, and relationship between, serum markers of brain injury [neurofilament light (NfL), glial fibrillary acidic protein (GFAP) and total tau] and markers of dysregulated host response (autoantibody production and cytokine profiles) in 175 patients admitted with COVID-19 and 45 patients with influenza. During hospitalization, sera from patients with COVID-19 demonstrated elevations of NfL and GFAP in a severity-dependent manner, with evidence of ongoing active brain injury at follow-up 4 months later. These biomarkers were associated with elevations of pro-inflammatory cytokines and the presence of autoantibodies to a large number of different antigens. Autoantibodies were commonly seen against lung surfactant proteins but also brain proteins such as myelin associated glycoprotein. Commensurate findings were seen in the influenza cohort. A distinct process characterized by elevation of serum total tau was seen in patients at follow-up, which appeared to be independent of initial disease severity and was not associated with dysregulated immune responses unlike NfL and GFAP. These results demonstrate that brain injury is a common consequence of both COVID-19 and influenza, and is therefore likely to be a feature of severe viral infection more broadly. The brain injury occurs in the context of dysregulation of both innate and adaptive immune responses, with no single pathogenic mechanism clearly responsible. Needham et al. reveal elevations in blood biomarkers of brain injury in patients hospitalised with COVID-19. The changes, which were severity-dependent, were associated with dysregulated immune responses including increases in pro-inflammatory cytokines and autoantibodies. Ongoing active brain injury could still be seen months after infection.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Medicinska och farmaceutiska grundvetenskaperx Neurovetenskaper0 (SwePub)301052 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Basic Medicinex Neurosciences0 (SwePub)301052 hsv//eng
653 a COVID-19
653 a brain injury
653 a neuroinflammation
653 a autoantibodies
653 a infection
653 a Neurosciences & Neurology
700a Ren, A. L.4 aut
700a Digby, R. J.4 aut
700a Norton, E. J.4 aut
700a Ebrahimi, S.4 aut
700a Outtrim, J. G.4 aut
700a Chatfield, D. A.4 aut
700a Manktelow, A. E.4 aut
700a Leibowitz, M. M.4 aut
700a Newcombe, V. F. J.4 aut
700a Doffinger, R.4 aut
700a Barcenas-Morales, G.4 aut
700a Fonseca, C.4 aut
700a Taussig, M. J.4 aut
700a Burnstein, R. M.4 aut
700a Samanta, R. J.4 aut
700a Dunai, C.4 aut
700a Sithole, N.4 aut
700a Ashton, Nicholas J.u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xashtn
700a Zetterberg, Henrik,d 1973u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi,Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry4 aut0 (Swepub:gu)xzethe
700a Gisslén, Magnus,d 1962u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för infektionssjukdomar,Institute of Biomedicine, Department of Infectious Medicine4 aut0 (Swepub:gu)xgissm
700a Edén, Arvid,d 1975u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för infektionssjukdomar,Institute of Biomedicine, Department of Infectious Medicine4 aut0 (Swepub:gu)xedear
700a Marklund, Emelieu Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för infektionssjukdomar,Institute of Biomedicine, Department of Infectious Medicine4 aut0 (Swepub:gu)xmaeme
700a Openshaw, P. J. M.4 aut
700a Dunning, J.4 aut
700a Griffiths, M. J.4 aut
700a Cavanagh, J.4 aut
700a Breen, G.4 aut
700a Irani, S. R.4 aut
700a Elmer, A.4 aut
700a Kingston, N.4 aut
700a Summers, C.4 aut
700a Bradley, J. R.4 aut
700a Taams, L. S.4 aut
700a Michael, B. D.4 aut
700a Bullmore, E. T.4 aut
700a Smith, K. G. C.4 aut
700a Lyons, P. A.4 aut
700a Coles, A. J.4 aut
700a Menon, D. K.4 aut
710a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi4 org
773t Braind : Oxford University Press (OUP)g 145:11, s. 4097-4107q 145:11<4097-4107x 0006-8950x 1460-2156
8564 8u https://gup.ub.gu.se/publication/320574
8564 8u https://doi.org/10.1093/brain/awac321

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