# Profile of Tau-Associated Selected MicroRNAs in Hospitalized COVID-19 Patients: An Exploratory Single-Center Study

**Authors:** Elena Carbone, Maria Antonella Zingaropoli, Federica Perrone, Giuseppina Talarico, Patrizia Pasculli, Antonio Minni, Carla Petrella, Christian Barbato, Paola Piscopo

PMC · DOI: 10.3390/cells15060503 · 2026-03-12

## TL;DR

This study explores how certain microRNAs linked to tau proteins behave in hospitalized COVID-19 patients and finds they are elevated compared to healthy individuals.

## Contribution

The study is the first to quantify specific tau-associated microRNAs in hospitalized COVID-19 patients and assess their association with disease severity.

## Key findings

- All three miRNAs (miR-92a-3p, miR-320a, miR-320b) were elevated in hospitalized COVID-19 patients compared to healthy controls.
- miR-320b was significantly elevated only in severe cases of COVID-19.
- No significant correlations were found between miRNA levels and biomarkers of neuroinflammation or neurodegeneration.

## Abstract

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.

## Linked entities

- **Diseases:** COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** ORF1ab (ORF1a polyprotein;ORF1ab polyprotein) [NCBI Gene 43740578], MIR1915 (microRNA 1915) [NCBI Gene 100302129] {aka MIRN1915, hsa-mir-1915}, MMP2 (matrix metallopeptidase 2) [NCBI Gene 4313] {aka CLG4, CLG4A, MMP-2, MMP-II, MONA, TBE-1}, KRT18 (keratin 18) [NCBI Gene 3875] {aka CK-18, CYK18, K18}, APP (amyloid beta precursor protein) [NCBI Gene 351] {aka AAA, ABETA, ABPP, AD1, APPI, CTFgamma}, TIMP1 (TIMP metallopeptidase inhibitor 1) [NCBI Gene 7076] {aka CLGI, EPA, EPO, HCI, TIMP, TIMP-1}, MMP9 (matrix metallopeptidase 9) [NCBI Gene 4318] {aka CLG4B, GELB, MANDP2, MMP-9}, MIR320A (microRNA 320a) [NCBI Gene 407037] {aka MIRN320, MIRN320A, hsa-mir-320a, mir-320a}, NEFL (neurofilament light chain) [NCBI Gene 4747] {aka CMT1F, CMT2E, CMTDIG, NF-L, NF68, NFL}, MAPT (microtubule associated protein tau) [NCBI Gene 4137] {aka DDPAC, FTD1, FTDP-17, MAPTL, MSTD, MTBT1}, GFAP (glial fibrillary acidic protein) [NCBI Gene 2670] {aka ALXDRD}
- **Diseases:** central nervous system disorders (MESH:D002493), neurodegeneration (MESH:D019636), microvascular dysfunction (MESH:D017566), headache (MESH:D006261), IOT (MESH:D053717), diabetes (MESH:D003920), systemic disorder (MESH:D009422), dyspnea (MESH:D004417), ARDS (MESH:D012128), HC (MESH:D000067329), cognitive disturbances (MESH:D003072), cognitive symptoms (MESH:D019954), FTD (MESH:D057180), neuroinflammation (MESH:D000090862), cardiovascular diseases (MESH:D002318), AA (MESH:D004618), pneumonia (MESH:D011014), endothelial injury (MESH:D057772), paresthesia (MESH:D010292), syncope (MESH:D013575), injury to (MESH:D014947), neurocognitive decline (MESH:D060825), infection (MESH:D007239), axonal damage (MESH:D001480), inflammation (MESH:D007249), memory deficits (MESH:D008569), COVID-19 (MESH:D000086382), autonomic dysfunction (MESH:D001342), respiratory disease (MESH:D012140), fog (MESH:D005222), cough (MESH:D003371), AD (MESH:D000544), anosmia (MESH:D000857), NDs (MESH:D009461), amyloid abnormalities (MESH:C000718787), Infectious Diseases (MESH:D003141), fever (MESH:D005334), hypertension (MESH:D006973), Long COVID (MESH:D000094024), frontal syndrome (MESH:D020233), tissue damage (MESH:D017695), multiple sclerosis (MESH:D009103), impaired concentration (MESH:C567712), confusion (MESH:D003221), neurological injury (MESH:D020196), encephalopathy (MESH:D001927), viral infections (MESH:D014777), Hemolysis (MESH:D006461), vascular dysfunction (MESH:D002561)
- **Chemicals:** heparin (MESH:D006493), oxygen (MESH:D010100), water (MESH:D014867)
- **Species:** Homo sapiens (human, species) [taxon 9606], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Mus musculus (house mouse, species) [taxon 10090]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC13025435/full.md

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Source: https://tomesphere.com/paper/PMC13025435