MiRNA-501-3p and miRNA-502-3p: a promising biomarker panel for Alzheimer’s disease
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Abstract
Introduction: Alzheimer's disease (AD) lacks a less invasive and early detectable biomarker. Here, we investigated the biomarker potential of miR‐501‐3p and miR‐502‐3p using different AD sources. Methods: MiR‐501‐3p and miR‐502‐3p expressions were evaluated in AD cerebrospinal fluid (CSF) exosomes, serum exosomes, familial and sporadic AD fibroblasts and B‐lymphocytes by qRT‐PCR analysis. Further, miR‐501‐3p and miR‐502‐3p expressions were analysed in APP, Tau plasmid transfected cells media exosomes and in different brain cell types. Results: MiR‐501‐3p and miR‐502‐3p expressions were significantly up‐regulated in AD CSF exosomes relative to controls. MiRNA levels were high in accordance with amyloid plaque and NFT density in multiple brain regions. Similarly, both miRNAs were elevated in AD and MCI serum exosomes compared with controls. MiR‐502‐3p expression was high in familial AD and sporadic AD B‐lymphocytes. MiR‐501‐3p and miR‐502‐3p expression were elevated intracellularly and secreted extracellularly in response to APP and Tau pathology. Finally, neurons and astrocytes displayed high expression of these miRNAs. Discussion: These results suggest that miR‐501‐3p and miR‐502‐3p could be promising biomarkers for AD. Key points: MiR‐501‐3p and miR‐502‐3p expression is elevated in AD CSF exosomes, AD serum exosomes, AD B‐lymphocytes and Aβ‐ and Tau‐treated cells. MiR‐501‐3p and miR‐502‐3p are correlated with amyloid plaque and NFT tangle density in specific brain regions. MiR‐501‐3p and miR‐502‐3p are highly expressed in neurons and astrocytes, suggesting that these cells are the source of miRNA secretion. MiR‐501‐3p and miR‐502‐3p could be a promising biomarker panel for AD
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miRNAs expressed in endothelial and neurogenic niches, including miR-126, miR-501-3p, miR-502-3p, and miR-9, implicate post-transcriptional dysfunction in vascular integrity and adult neurogenesis.
“Furthermore, miRNAs expressed in endothelial and neurogenic niches, including miR-126 (tight-junction stability), miR-501-3p and miR-502-3p (CSF/exosomal biomarkers), and miR-9 (Notch/CAMKK2-regulated neurogenesis and context-dependent amyloid/vascular roles), implicate post-transcriptional dysfunction in vascular integrity and adult neurogenesis, with some mechanisms inferred from vascular injury”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Devara et al., 2025
miR-502-3p is part of a plasma and CSF miRNA panel that correlates with amyloid and tau burden in AD patients.
“Recent exosomal biomarker studies also identify miR-502-3p as part of a plasma and CSF miRNAs panel that correlates with amyloid and tau burden in AD patients (Devara et al., 2025).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Devara et al., 2025
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Kumbol, V., Ivanov, A., McGurran, H., Schüler, J., Zhai, Y., Ludwik, K., Hinkelmann, L., Brehm, M., Krüger, C., Küchler, J., et al. (2025) · Cell Communication and Signaling · doi:10.1186/s12964-025-02199-8 · Cited by 8 · see citing works
Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease
Donepudi, K., Eadha, S., Rodarte, D., Sharma, B., & Kumar, S. (2026) · Ageing Research Reviews · doi:10.1016/j.arr.2026.103211
Self-citation
- Authors
- Devara, D., Sharma, B., Goyal, G., Rodarte, D., Kulkarni, A., Tinu, N., Pai, A., & Kumar, S.
- Affiliations
- Center of Emphasis in Neuroscience Department of Molecular and Translational Medicine Paul L. Foster School of Medicine Texas Tech University Health Sciences Center El Paso El Paso Texas USA
- Venue
- Clinical and Translational Medicine
- Publisher
- Wiley
- Published
- 2025-07
- Volume
- 15
- Issue
- 7
- ISSN
- 2001-1326
- PMC
- PMC12238675
- Cited by
- 15
- References
- 3
- Language
- en
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