<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Needham EJ</submitter><funding>NIHR Cambridge Biomedical Centre</funding><funding>Brain Research UK</funding><funding>European Research Council</funding><funding>Medical Research Council</funding><funding>National Institute for Health Research (NIHR)</funding><funding>Rosetrees</funding><funding>Wellcome Trust</funding><funding>Academy of Medical Sciences</funding><pagination>4097-4107</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9494359</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>145(11)</volume><pubmed_abstract>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 demo</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses.</pubmed_title><pmcid>PMC9494359</pmcid><funding_grant_id>MR/R005036/1</funding_grant_id><funding_grant_id>ACF-2022-26-005</funding_grant_id><funding_grant_id>NIHR200256</funding_grant_id><funding_grant_id>NIHR201395</funding_grant_id><funding_grant_id>AMS-CSF4-Newcombe</funding_grant_id><funding_grant_id>COV-LT2-0004</funding_grant_id><funding_grant_id>090382/Z/09/Z</funding_grant_id><funding_grant_id>MR/V03605X/1</funding_grant_id><funding_grant_id>M957</funding_grant_id><funding_grant_id>104079/Z/14/Z</funding_grant_id><funding_grant_id>MR/V007181/1</funding_grant_id><funding_grant_id>720931</funding_grant_id><funding_grant_id>CL-2018-14-001</funding_grant_id><funding_grant_id>ACF-2009-14-007</funding_grant_id><funding_grant_id>MR/V007173/1</funding_grant_id><funding_grant_id>NF-SI-0513-10051</funding_grant_id><funding_grant_id>MR/T028750/1</funding_grant_id><funding_grant_id>681712</funding_grant_id><funding_grant_id>COVID-19-RECPLAS</funding_grant_id><funding_grant_id>201819-20</funding_grant_id><funding_grant_id>MC_G0802534</funding_grant_id><pubmed_authors>Samanta 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AM</pubmed_authors><pubmed_authors>Fuller S</pubmed_authors><pubmed_authors>Vergese B</pubmed_authors><pubmed_authors>Cooper D</pubmed_authors><pubmed_authors>Coudert JD</pubmed_authors><pubmed_authors>Matheson NJ</pubmed_authors><pubmed_authors>Barcenas-Morales G</pubmed_authors><pubmed_authors>Graves B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Brain injury in COVID-19 is associated with dysregulated innate and adaptive immune responses.</name><description>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 demo</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-06-18T07:02:17.852Z</modification><creation>2025-04-07T09:57:33.429Z</creation></dates><accession>S-EPMC9494359</accession><cross_references><pubmed>36065116</pubmed><doi>10.1093/brain/awac321</doi></cross_references></HashMap>