ArticleFrontiers in immunology2026
MiR-34a deficiency enhances nucleic acid sensing and type I IFN signaling in a mouse model of Alzheimer's disease.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Systemic Molecular Alterations ofInternational journal of molecular sciences · 2026Article
- Blood-brain barrier dysfunction and peripheral immune activation in Alzheimer's disease: an inflammation-centered review.Frontiers in immunology · 2026Review
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6 authors.
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Abstract
Background: A number of microRNAs are implicated in aging, cell senescence, inflammation, and neurodegenerative diseases. Particularly, miR-34a levels in the brain are increased in Alzheimer's disease (AD) but its mechanistic role in AD pathogenesis is unknown. Methods: In order to investigate the role of miR-34a in AD, we produced an AD mouse model, Tg-SwDI mice, with whole body/constitutive miR-34a knockout (KO). Their cognitive function was evaluated by Morris water maze. Immunohistochemistry and immunofluorescence were used for neuropathological evaluation. Bulk RNA-seq followed by bioinformatics was used for hippocampal transcriptomics. The effect of miR-34a knockdown on expression of interferon-stimulated genes (ISG) was determined using cultured microglial cells and quantitative PCR. Results: MiR-34a KO improved long-term memory in Tg-SwDI mice, which was associated with decreases in the ratio of insoluble Aβ42 to Aβ40 and with increases in soluble and insoluble Aβ40 in the cerebral cortex. Anti-Iba1 immunofluorescence revealed increases in activated microglia. Bulk RNA-sequencing of the hippocampus followed by a gene set enrichment analysis (Enrichr) identified "cellular response to type I interferon" and "type I interferon signaling pathway" as the most prominent gene sets in miR-34a KO Tg-SwDI mice compared to miR-34a wild-type Tg-SwDI mice. Many interferon-stimulated genes (ISGs) that characterize interferon responsive microglia (IRM) were upregulated in miR-34a KO Tg-SwDI mice. MiR-34a knockdown strongly enhanced ISGs expression in TLR7 ligand-stimulated BV2 and primary microglia. Conclusion: Our results suggest that miR-34a inhibits the transition of microglia to the IRM state that may modulate synaptic and cognitive functions in neurodegenerative diseases and aging.
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