ArticleBrain, behavior, & immunity - health2024
Changes in neuroinflammatory biomarkers correlate with disease severity and neuroimaging alterations in patients with COVID-19 neurological complications.
Article in Brain, behavior, & immunity - health, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Neuropsychiatric Involvement in Hospitalized COVID-19 Is Embedded in Multi-Organ Disease: A Retrospective Five-Axis Record-Derived Phenotype Atlas with Renal-Urinary Prognostic Dominance.Pathogens (Basel, Switzerland) · 2026Article
- Proteomic Analysis of Cerebrospinal Fluid from Severe COVID-19 Patients Reveals Prognostic Biomarkers Associated with Disease Outcome.Proteomics. Clinical applications · 2026Article
- Factors associated with severe neurological sequelae of COVID-19: findings from the multicenter COVID-BRAIN imaging cohort.Frontiers in human neuroscience · 2026Article
- Comparison of cerebrospinal fluid biomarkers in patients with severe COVID-19 neurological outcomes and Alzheimer's disease.Brain, behavior, & immunity - health · 2025Article
- Clinical and radiological characteristics and 1-year self-reported outcomes from patients with encephalitis and coronavirus disease 2019.Journal of medical case reports · 2025Observational
- Article
- Neurological Complications of COVID-19: Unraveling the Pathophysiological Underpinnings and Therapeutic Implications.Viruses · 2024Review
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22 authors.
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Abstract
COVID-19 induces acute and persistent neurological symptoms in mild and severe cases. Proposed concomitant mechanisms include direct viral infection and strain, coagulopathy, hypoxia, and neuroinflammation. However, underlying molecular alterations associated with multiple neurological outcomes in both mild and severe cases are majorly unexplored. To illuminate possible mechanisms leading to COVID-19 neurological disease, we retrospectively investigated in detail a cohort of 35 COVID-19 mild and severe hospitalized patients presenting neurological alterations subject to clinically indicated cerebrospinal fluid (CSF) sampling. Clinical and neurological investigation, brain imaging, viral sequencing, and cerebrospinal CSF analyses were carried out. We found that COVID-19 patients presented heterogeneous neurological symptoms dissociated from lung burden. Nasal swab viral sequencing revealed a dominant strain at the time of the study, and we could not detect traces of SARS-CoV-2's spike protein in patients' CSF by multiple reaction monitoring analysis. Patients presented ubiquitous systemic hyper-inflammation and broad alterations in CSF proteomics related to inflammation, innate immunity, and hemostasis, irrespective of COVID-19 severity or neuroimaging alterations. Elevated CSF interleukin-6 (IL6) correlated with disease severity (sex-, age-, and comorbidity-adjusted mean Severe 24.5 pg/ml, 95% confidence interval (CI) 9.62-62.23 vs. Mild 3.91 pg/mL CI 1.5-10.3 patients, p = 0.019). CSF tumor necrosis factor-alpha (TNFα) and IL6 levels were higher in patients presenting pronounced neuroimaging alterations compared to those who did not (sex-, age-, and comorbidity-adjusted mean TNFα Pronounced 3.4, CI 2.4-4.4 vs. Non-Pronounced 2.0, CI 1.4-2.5, p = 0.022; IL6 Pronounced 33.11, CI 8.89-123.31 vs Non-Pronounced 6.22, CI 2.9-13.34, p = 0.046). Collectively, our findings put neuroinflammation as a possible driver of COVID-19 acute neurological disease in mild and severe cases.
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