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Cerebrospinal fluid biomarkers in SARS-CoV-2 patients with acute neurological syndromes

BACKGROUND AND PURPOSE: Mechanisms underlying acute brain injury in SARS-CoV-2 patients remain poorly understood. A better characterization of such mechanisms remains essential to preventing long-term neurological sequelae. Our present aim was to study a panel of biomarkers of neuroinflammation and...

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Detalles Bibliográficos
Autores principales: Chaumont, H., Kaczorowski, F., San-Galli, A., Michel, P.P., Tressières, B., Roze, E., Quadrio, I., Lannuzel, A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier Masson SAS. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9708608/
https://www.ncbi.nlm.nih.gov/pubmed/36610823
http://dx.doi.org/10.1016/j.neurol.2022.11.002
Descripción
Sumario:BACKGROUND AND PURPOSE: Mechanisms underlying acute brain injury in SARS-CoV-2 patients remain poorly understood. A better characterization of such mechanisms remains essential to preventing long-term neurological sequelae. Our present aim was to study a panel of biomarkers of neuroinflammation and neurodegeneration in the cerebrospinal fluid (CSF) of NeuroCOVID patients. METHODS: We retrospectively collected clinical and CSF biomarkers data from 24 NeuroCOVID adults seen at the University Hospital of Guadeloupe between March and June 2021. RESULTS: Among 24 NeuroCOVID patients, 71% had encephalopathy and 29% meningoencephalitis. A number of these patients also experienced de novo movement disorder (33%) or stroke (21%). The CSF analysis revealed intrathecal immunoglobulin synthesis in 54% of NeuroCOVID patients (two with a type 2 pattern and 11 with a type 3) and elevated neopterin levels in 75% of them (median 9.1 nM, IQR 5.6–22.1). CSF neurofilament light chain (NfL) was also increased compared to a control group of non-COVID-19 patients with psychiatric illnesses (2905 ng/L, IQR 1428–7124 versus 1222 ng/L, IQR 1049–1566). Total-tau was elevated in the CSF of 24% of patients, whereas protein 14-3-3, generally undetectable, reached intermediate levels in two patients. Finally, CSF Aß1-42 was reduced in 52.4% of patients (median 536 ng/L, IQR 432–904) with no change in the Aß1-42/Aß1-40 ratio (0.082, IQR 0.060–0.096). CONCLUSIONS: We showed an elevation of CSF biomarkers of neuroinflammation in NeuroCOVID patients and a rise of CSF NfL, evocative of neuronal damage. However, longitudinal studies are needed to determine whether NeuroCOVID could evolve into a chronic neurodegenerative condition.