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dc.contributor.authorKyaw, Sandar
dc.date.accessioned2024-01-31T16:18:53Z
dc.date.available2024-01-31T16:18:53Z
dc.date.issued2023
dc.identifier.citationNeedham, E. J., Tharmaratnam, K., Williams, R., Huang, Y., Boardman, S. A., Sharma, P., Subramaniam, K., Digby, R., Ren, A., Norton, E., et al. (2023). Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses. Nature Communications, 14, pp.8487.en_US
dc.identifier.other10.1038/s41467-023-42320-4
dc.identifier.urihttp://hdl.handle.net/20.500.12904/18191
dc.descriptionOpen Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
dc.description.abstractTo understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1-11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely. Copyright © 2023, The Author(s).
dc.description.urihttps://www.nature.com/articles/s41467-023-42320-4en_US
dc.formatFull text uploaded
dc.language.isoenen_US
dc.subjectCOVID-19en_US
dc.subjectBrain injuriesen_US
dc.titlePara-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responsesen_US
dc.typeArticleen_US
rioxxterms.funderDefault funderen_US
rioxxterms.identifier.projectDefault projecten_US
rioxxterms.versionNAen_US
rioxxterms.typeJournal Article/Reviewen_US
refterms.dateFOA2024-01-31T16:18:54Z
refterms.panelUnspecifieden_US
refterms.dateFirstOnline2023-12-22
html.description.abstractTo understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1-11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely.<br/>Copyright &#xa9; 2023, The Author(s).en_US
rioxxterms.funder.project94a427429a5bcfef7dd04c33360d80cden_US


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