Edward J. Needham,, Alexander L. Ren, Richard J. Digby, Emma J. Norton, Soraya Ebrahimi, Joanne G. Outtrim, Doris A. Chatfield, Anne E. Manktelow, Maya M. Leibowitz, Virginia F. J. Newcombe, Rainer Doffinger, Gabriela Barcenas-Morales, Claudia Fonseca, Michael J. Taussig, Rowan M. Burnstein, Romit J. Samanta, Cordelia Dunai, Nyarie Sithole, Nicholas J. Ashton, Henrik Zetterberg, Magnus Gisslén, Arden Edén,, Emelie Marklund, Peter J. M. Openshaw, Jake Dunning, Michael J. Griffiths, Jonathan Cavanagh, Gerome Breen, Sarosh R. Irani,, Anne Elmer, Nathalie Kingston,, Charlotte Summers,, John R. Bradley,, Leonie S. Taams, Benedict D. Michael, Edward T. Bullmore, Kenneth G. C. Smith, Paul A. Lyons, Alasdair J. Coles, David K. Menon and the Cambridge NeuroCOVID Group, the CITIID-NIHR COVID- BioResource Collaboration and Cambridge NIHR Clinical Research Facility
6 September 2022
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.
Researchers 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.