tetano
Editor, Senior Moderator
Cells
. 2026 Mar 12;15(6):503.
doi: 10.3390/cells15060503.
Profile of Tau-Associated Selected MicroRNAs in Hospitalized COVID-19 Patients: An Exploratory Single-Center Study
Elena Carbone[SUP] 1 [/SUP], Maria Antonella Zingaropoli[SUP] 2 [/SUP], Federica Perrone[SUP] 3 [/SUP], Giuseppina Talarico[SUP] 4 [/SUP], Patrizia Pasculli[SUP] 2 [/SUP], Antonio Minni[SUP] 5 6 7 [/SUP], Carla Petrella[SUP] 8 [/SUP], Christian Barbato[SUP] 8 [/SUP], Paola Piscopo[SUP] 1 [/SUP]
Affiliations
Tau-associated microRNAs have been implicated in neurodegenerative disorders, yet their behavior during SARS-CoV-2 infection remains insufficiently understood. The aim of this study was to quantify circulating levels of miR-92a-3p, miR-320a, and miR-320b in hospitalized COVID-19 patients and evaluate their relationship with disease severity and established biomarkers of neuroinflammation and neurodegeneration. We conducted a retrospective single-center study including 38 hospitalized COVID-19 patients and 12 healthy controls. MicroRNA plasma levels were quantified by RT-qPCR. Patients were stratified by ARDS severity and ventilation requirements. Correlations between miRNAs and previously published biomarkers were examined. All three miRNAs were elevated in COVID-19 patients compared to healthy controls. miR-92a-3p and miR-320a were increased in both severe and non-severe cases, while miR-320b was significantly elevated only in severe disease. No statistically significant correlations were observed between miRNA levels and NfL, GFAP, MMP-9, or other biomarkers in COVID-19 patients. Tau-associated circulating microRNAs appear dysregulated in acute SARS-CoV-2 infection, but their relationship to neurological injury remains unclear. These findings are preliminary and require validation in larger, longitudinal cohorts with standardized neurological outcomes.
Keywords: COVID-19; circulating microRNAs; miR-320a; miR-320b; miR-92a-3p; neurodegeneration; neuroinflammation; plasma biomarkers; tau pathway.
. 2026 Mar 12;15(6):503.
doi: 10.3390/cells15060503.
Profile of Tau-Associated Selected MicroRNAs in Hospitalized COVID-19 Patients: An Exploratory Single-Center Study
Elena Carbone[SUP] 1 [/SUP], Maria Antonella Zingaropoli[SUP] 2 [/SUP], Federica Perrone[SUP] 3 [/SUP], Giuseppina Talarico[SUP] 4 [/SUP], Patrizia Pasculli[SUP] 2 [/SUP], Antonio Minni[SUP] 5 6 7 [/SUP], Carla Petrella[SUP] 8 [/SUP], Christian Barbato[SUP] 8 [/SUP], Paola Piscopo[SUP] 1 [/SUP]
Affiliations
- PMID: 41892294
- PMCID: PMC13025435
- DOI: 10.3390/cells15060503
Tau-associated microRNAs have been implicated in neurodegenerative disorders, yet their behavior during SARS-CoV-2 infection remains insufficiently understood. The aim of this study was to quantify circulating levels of miR-92a-3p, miR-320a, and miR-320b in hospitalized COVID-19 patients and evaluate their relationship with disease severity and established biomarkers of neuroinflammation and neurodegeneration. We conducted a retrospective single-center study including 38 hospitalized COVID-19 patients and 12 healthy controls. MicroRNA plasma levels were quantified by RT-qPCR. Patients were stratified by ARDS severity and ventilation requirements. Correlations between miRNAs and previously published biomarkers were examined. All three miRNAs were elevated in COVID-19 patients compared to healthy controls. miR-92a-3p and miR-320a were increased in both severe and non-severe cases, while miR-320b was significantly elevated only in severe disease. No statistically significant correlations were observed between miRNA levels and NfL, GFAP, MMP-9, or other biomarkers in COVID-19 patients. Tau-associated circulating microRNAs appear dysregulated in acute SARS-CoV-2 infection, but their relationship to neurological injury remains unclear. These findings are preliminary and require validation in larger, longitudinal cohorts with standardized neurological outcomes.
Keywords: COVID-19; circulating microRNAs; miR-320a; miR-320b; miR-92a-3p; neurodegeneration; neuroinflammation; plasma biomarkers; tau pathway.