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Serum and cerebrospinal fluid biomarker profiles in acute SARS-CoV-2-associated neurological syndromes.
Paterson, Ross W; Benjamin, Laura A; Mehta, Puja R; Brown, Rachel L; Athauda, Dilan; Ashton, Nicholas J; Leckey, Claire A; Ziff, Oliver J; Heaney, Judith; Heslegrave, Amanda J; Benedet, Andrea L; Blennow, Kaj; Checkley, Anna M; Houlihan, Catherine F; Mummery, Catherine J; Lunn, Michael P; Manji, Hadi; Zandi, Michael S; Keddie, Stephen; Chou, Michael; Vinayan Changaradil, Deepthi; Solomon, Tom; Keshavan, Ashvini; Barker, Suzanne; Jäger, Hans Rolf; Carletti, Francesco; Simister, Robert; Werring, David J; Spyer, Moira J; Nastouli, Eleni; Gauthier, Serge; Rosa-Neto, Pedro; Zetterberg, Henrik; Schott, Jonathan M.
  • Paterson RW; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Benjamin LA; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Mehta PR; Darent Valley Hospital, Dartford, Kent DA2 8DA, UK.
  • Brown RL; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Athauda D; UCL Institute of Neurology, Stroke Research Centre, Russell Square House, London WC1B 5EH, UK.
  • Ashton NJ; University of Liverpool, Brain Infections Group, Liverpool, Merseyside L69 3GA, UK.
  • Leckey CA; Laboratory of Molecular and Cell Biology, UCL, London WC1E 6BT, UK.
  • Ziff OJ; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Heaney J; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Heslegrave AJ; University College London Institute of Immunity and Transplantation, London NW3 2QG, UK.
  • Benedet AL; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Blennow K; Francis Crick Institute, London NW1 1AT, UK.
  • Checkley AM; Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal 431 41, Sweden.
  • Houlihan CF; King's College London, Institute of Psychiatry, Psychology & Neuroscience, Maurice Wohl Clinical Neuroscience Institute, London SE5 9RT, UK.
  • Mummery CJ; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Lunn MP; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Manji H; Francis Crick Institute, London NW1 1AT, UK.
  • Zandi MS; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Keddie S; Advanced Pathogens Diagnostic Unit, University College London Hospitals NHS Foundation Trust, London WC1H 8NJ, UK.
  • Chou M; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Vinayan Changaradil D; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Solomon T; UK Dementia Research Institute, London WC1E 6BT, UK.
  • Keshavan A; Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal 431 41, Sweden.
  • Barker S; Department of Psychiatry and Neurochemistry, Institute of Neuroscience & Physiology, the Sahlgrenska Academy at the University of Gothenburg, Mölndal 431 41, Sweden.
  • Jäger HR; Department of Infection and Immunity, University College London, London WC1E 6BT, UK.
  • Carletti F; Hospital for Tropical Diseases, University College Hospitals London, London WC1E 6BT, UK.
  • Simister R; Department of Infection and Immunity, University College London, London WC1E 6BT, UK.
  • Werring DJ; Department of Clinical Virology, University College London Hospitals NHS Foundation Trust, London WC1H 8NJ, UK.
  • Spyer MJ; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Nastouli E; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Gauthier S; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Rosa-Neto P; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
  • Zetterberg H; University College London, Queen Square Institute of Neurology, London WC1N 3BG, UK.
  • Schott JM; National Hospital for Neurology and Neurosurgery, University College London Hospitals NHS Foundation Trust, Queen Square, London WC1N 3BG, UK.
Brain Commun ; 3(3): fcab099, 2021.
Article in English | MEDLINE | ID: covidwho-1358433
ABSTRACT
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-Barré 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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Full text: Available Collection: International databases Database: MEDLINE Type of study: Experimental Studies / Observational study / Randomized controlled trials Language: English Journal: Brain Commun Year: 2021 Document Type: Article Affiliation country: Braincomms

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Full text: Available Collection: International databases Database: MEDLINE Type of study: Experimental Studies / Observational study / Randomized controlled trials Language: English Journal: Brain Commun Year: 2021 Document Type: Article Affiliation country: Braincomms