ArticleACS omega2025
Cerebrospinal Fluid Proteomic Profiling Reveals Proteins Associated with Neuroinflammatory Response in COVID-19 Patients.
Article in ACS omega, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Machine Learning Identification of Cell-Type-Specific Molecular Signatures Distinguishing COVID-19 from Other Lower Respiratory Tract Diseases.Life (Basel, Switzerland) · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The COVID-19 pandemic has highlighted the diverse clinical manifestations of SARS-CoV-2 infection, including neurological complications. This study investigates cerebrospinal fluid (CSF) proteomic profiles to identify proteins associated with neuroinflammatory processes in COVID-19. CSF samples from 11 critically ill patients and 5 COVID-19-negative controls were analyzed using high-resolution liquid chromatography-tandem mass spectrometry. A total of 203 proteins were identified, of which 76 exhibited differential expression peptides (DEPs). Proteins involved in coagulation (fibrinogen alpha and beta chains, prothrombin) and immune responses (complement cascade components, immunoglobulin heavy constant gamma, kappa, and lambda subunits) were significantly upregulated in COVID-19 patients. In contrast, proteins involved in antioxidant defense (e.g., superoxide dismutase) and neural maintenance (e.g., neural cell adhesion molecule 1, Neuronal cell adhesion molecule) were significantly downregulated. Functional annotation revealed enriched pathways associated with hemostasis, immune regulation, and neuroinflammatory responses. Protein-protein interaction analysis highlighted interactions among complement and coagulation cascade components, underscoring their roles in inflammation and potential thrombotic complications. These findings suggest that SARS-CoV-2 infection induces significant alterations in the CSF proteome, reflecting neuroinflammatory and oxidative stress mechanisms. Identifying these proteins and their association with diverse pathophysiological mechanisms provides insights into the neurological impact of COVID-19 and may serve as therapeutic targets and potential biomarkers. Further studies are needed to validate these findings and explore their clinical implications in post-COVID-19 neurological syndromes.
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Registered trials
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