Biomarkers of Neurological Damage: From Acute Stage to Post-Acute Sequelae of COVID-19
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Background: Neurological symptoms (NS) in COVID-19 are related to both acute stage and long-COVID. We explored levels of brain injury biomarkers (NfL and GFAP) and myeloid activation marker (sCD163) and their implications on the CNS. Materials and Methods: In hospitalized COVID-19 patients plasma samples were collected at two time points: on hospital admission (baseline) and three months after hospital discharge (Tpost). Patients were stratified according to COVID-19 severity based on acute respiratory distress syndrome (ARDS) onset (severe and non-severe groups). A further stratification according to the presence of NS (with and without groups) at baseline (requiring a puncture lumbar for diagnostic purposes) and according to NS self-referred at Tpost was performed. Finally, cerebrospinal fluid (CSF) samples were collected from patients with NS present at baseline. Results: We enrolled 144 COVID-19 patients (62 female/82 male; median age [interquartile range, IQR]): 64 [55–77]) and 53 heathy donors (HD, 30 female/23 male; median age [IQR]: 64 [59–69]). At baseline, higher plasma levels of NfL, GFAP and sCD163 in COVID-19 patients compared to HD were observed (p < 0.0001, p < 0.0001 and p < 0.0001, respectively), especially in those with severe COVID-19 (p < 0.0001, p < 0.0001 and p < 0.0001, respectively). Patients with NS showed higher plasma levels of NfL, GFAP and sCD163 compared to those without (p = 0.0023, p < 0.0001 and 0.0370, respectively). At baseline, in COVID-19 patients with NS, positive correlations between CSF levels of sCD163 and CSF levels of NfL (ρ = 0.7536, p = 0.0017) and GFAP were observed (ρ = 0.7036, p = 0.0045). At Tpost, the longitudinal evaluation performed on 77 COVID-19 patients showed a significant reduction in plasma levels of NfL, GFAP and sCD163 compared to baseline (p < 0.0001, p < 0.0001 and p = 0.0413, respectively). Finally, at Tpost, in the severe group, higher plasma levels of sCD163 in patients with NS compared to those without were reported (p < 0.0001). Conclusions: High plasma levels of NfL, GFAP and sCD163 could be due to a proinflammatory systemic and brain response involving microglial activation and subsequent CNS damage. Our data highlight the association between myeloid activation and CNS perturbations.
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In a study examining patients three months after COVID-19 infection, there was an elevation in AD biomarkers like neurofilament light chain protein (NfL) and Glial Fibrillary Acidic Protein (GFAP), as well as sCD163 expression.
“In another study [84] which examined patients three months after COVID-19 infection, there was an elevation in AD biomarkers like neurofilament light chain protein (NfL) and Glial Fibrillary Acidic Protein (GFAP), as well as sCD163 expression.”
From What would it take to prove that a chronic infection is a causal agent in Alzheimer’s disease? (2025) · cites this paper as [84]
Results §3.4 reports that NfL, GFAP and sCD163 plasma levels remained higher than in healthy donors at follow-up, although all three had fallen from baseline. The follow-up was three months after hospital discharge, not three months after infection. The paper calls NfL and GFAP brain-injury biomarkers and sCD163 a myeloid-activation marker; it does not characterize them here as AD biomarkers. (LLM, conf=0.86)
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Self-citationLong-term neurological and otolaryngological sequelae of COVID-19: a retrospective study
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A perspective on pathogenesis of post-COVID syndrome
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A relação entre COVID-19 e tontura: uma revisão de literatura
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- Authors
- Zingaropoli, M. A., Pasculli, P., Barbato, C., Petrella, C., Fiore, M., Dominelli, F., Latronico, T., Ciccone, F., Antonacci, M., Liuzzi, G. M., Talarico, G., Bruno, G., Galardo, G., Pugliese, F., Lichtner, M., Mastroianni, C. M., Minni, A., & Ciardi, M. R.
- Affiliations
- Sapienza University of Rome (IT)
- National Research Council (IT)
- University of Bari Aldo Moro (IT)
- Policlinico Umberto I (IT)
- Ospedale Santa Maria Goretti (IT)
- Corresponding author
- Zingaropoli, Maria Antonella
- ORCID
- Zingaropoli, Maria Antonella
- Pasculli, Patrizia
- Barbato, Christian
- Petrella, Carla
- Fiore, Marco
- Dominelli, Federica
- Latronico, Tiziana
- Antonacci, Michele
- Liuzzi, Grazia Maria
- Talarico, Giuseppina
- Bruno, Giuseppe
- Galardo, Gioacchino
- Pugliese, Francesco
- Lichtner, Miriam
- Mastroianni, Claudio Maria
- Minni, Antonio
- Ciardi, Maria Rosa
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2023-09-13
- Volume
- 12
- Issue
- 18
- Pages
- 2270
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC10526816
- OpenAlex
- W4386746199
- Cited by
- 16
- References
- 68
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 3 · 2023: 1
- FWCI
- 2.72
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- BANCA D’ITALIA (0000625)
- Topics
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
- Health Sciences › Medicine › Infectious Diseases › Infectious Encephalopathies and Encephalitis
- Keywords
- COVID-19 pandemic, neurological symptoms, long COVID, neuroinflammation biomarkers, neurofilament light chain, glial fibrillary acidic protein, soluble CD163, myeloid activation, cerebrospinal fluid, plasma biomarkers, acute respiratory distress syndrome, post-acute sequelae, neurodegeneration
- MeSH terms
- COVID-19, Post-Acute COVID-19 Syndrome, Brain, Female, Humans, Male, Biomarkers, Disease Progression
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