期刊
BRAIN COMMUNICATIONS
卷 3, 期 3, 页码 -出版社
OXFORD UNIV PRESS
DOI: 10.1093/braincomms/fcab099
关键词
COVID-19; NfL; encephalitis; ADEM
资金
- University College London Hospitals National Institute for Health Research Biomedical Research Centre
- UCL Queen Square Biomedical Research Centre (BRC)
- Moorfields BRC [560441, 557595]
- Alzheimer's Association Clinician Scientist Fellowship [AACSF-20-685780]
- UK Dementia Research Institute
- Global Challenges Research Fund
- Wellcome Trust Fellowship [222102/Z/20/Z]
- Wolfson Clinical Research fellowship
- Weston Brain Institute [UB170045]
- Medical Research Council (MRC) Clinical Research Training Fellowship
- Swedish Research Council [2018-02532, 2017-00915]
- Alzheimer Drug Discovery Foundation (ADDF), USA [201809-2016862, RDAPB-201809-2016615]
- Swedish Alzheimer Foundation [AF-742881]
- Hjarnfonden, Sweden [FO2017-0243]
- European Union Joint Program for Neurodegenerative Disorders [JPND2019-466-236]
- European Research Council [681712]
- Swedish State Support for Clinical Research [ALFGBG-720931]
- UK Dementia Research Institute at UCL
- Weston Brain Institute
- Canadian Institutes of Health Research (CIHR) (FRN) [152985]
- Fonds de Recherche du Quebec-Sante (FRQS) [2020-VICO-279314]
- Swedish government [ALFGBG-715986]
- Swedish County Councils, the ALF-agreement [ALFGBG-715986]
- Wellcome Trust [222102/Z/20/Z] Funding Source: Wellcome Trust
Preliminary data on pathological and biomarkers indicate that SARS-CoV-2 infection may damage the nervous system, particularly causing CNS inflammation. Elevated levels of serum neurofilament light were found in COVID-19 patients, but not in community cases, suggesting potential peripheral nerve damage in response to severe illness rather than significant neurological damage. Astrocytic activation does not appear to be a major mediator of neuronal damage in COVID-19.
Preliminary pathological and biomarker data suggest that SARS-CoV-2 infection can damage the nervous system. To understand what, where and how damage occurs, we collected serum and CSF from patients with COVID-19 and characterized neurological syndromes involving the PNS and CNS (n = 34). We measured biomarkers of neuronal damage and neuroinflammation, and compared these with non-neurological control groups, which included patients with (n = 94) and without (n = 24) COVID-19. We detected increased concentrations of neurofilament light, a dynamic biomarker of neuronal damage, in the CSF of those with CNS inflammation (encephalitis and acute disseminated encephalomyelitis) [14 800 pg/ml (400, 32 400)], compared to those with encephalopathy [1410 pg/ml (756, 1446)], peripheral syndromes (Guillain-Barre syndrome) [740 pg/ml (507, 881)] and controls [872 pg/ml (654, 1200)]. Serum neurofilament light levels were elevated across patients hospitalized with COVID-19, irrespective of neurological manifestations. There was not the usual close correlation between CSF and serum neurofilament light, suggesting serum neurofilament light elevation in the non-neurological patients may reflect peripheral nerve damage in response to severe illness. We did not find significantly elevated levels of serum neurofilament light in community cases of COVID-19 arguing against significant neurological damage. Glial fibrillary acidic protein, a marker of astrocytic activation, was not elevated in the CSF or serum of any group, suggesting astrocytic activation is not a major mediator of neuronal damage in COVID-19.
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