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@ARTICLE{McGurran:284348,
      author       = {McGurran, Hugo and Graceffo, Eugenio and Kumbol, Victor and
                      Jendrach, Marina and Hinkelmann, Lukas and Brehm, Mariam and
                      Ravatt, Leandre and Krüger, Christina and Wallach, Thomas
                      and Haake, Alexander and Wegmann, Susanne and Heppner, Frank
                      L and Schülke, Markus and Lehnardt, Seija},
      title        = {{M}icro{RNA}-29a-5p contributes to neuroinflammation
                      through {TLR}7.},
      journal      = {Journal of neuroinflammation},
      volume       = {23},
      number       = {1},
      issn         = {1742-2094},
      address      = {London},
      publisher    = {BioMed Central},
      reportid     = {DZNE-2026-00119},
      pages        = {38},
      year         = {2026},
      abstract     = {MicroRNAs (miRNAs) canonically regulate
                      post-transcriptional gene expression, but they can also
                      serve as ligands for Toll-like receptors (TLRs). These
                      receptors and their associated signalling pathways
                      contribute to inflammatory responses involved in various
                      central nervous system (CNS) diseases, including Alzheimer's
                      disease (AD). Here, we investigated the effects of
                      extracellularly delivered miRNA in the context of
                      neuroinflammation. We identified several miRNAs specifically
                      dysregulated in AD and/or neuroinflammatory states, which
                      directly activate the single-stranded RNA sensors mouse TLR7
                      and human TLR7/8. Among them, extracellular miR-29a-5p
                      induced cytokine and chemokine release from murine primary
                      microglia, altered expression of TLR signalling elements,
                      and enhanced Aβ phagocytosis. Furthermore, this miRNA
                      induced neuronal injury dependent on microglial TLR7
                      expression, but also in a cell-autonomous fashion, in vitro.
                      Intrathecal injection of miR-29a-5p into mice led to
                      microglial accumulation and neuronal injury in the cerebral
                      cortex through TLR7 after 3 days. Brains of wild-type and
                      APP/PS1 mice, an established AD mouse model, treated with
                      multiple intrathecal miR-29a-5p injections over 120 days
                      exhibited changes in cytokine/chemokine expression and
                      neuronal injury. RNAseq analysis of the cerebral cortex of
                      both miRNA-treated genotypes revealed downregulation of
                      MAPK-associated pathways.Our study establishes AD-associated
                      miRNAs such as miR-29a-5p as TLR7 agonists and signalling
                      molecules for microglia, thereby altering the
                      neuroinflammatory response.},
      keywords     = {Animals / MicroRNAs: metabolism / MicroRNAs: genetics /
                      MicroRNAs: administration $\&$ dosage / Toll-Like Receptor
                      7: metabolism / Toll-Like Receptor 7: genetics / Mice /
                      Neuroinflammatory Diseases: metabolism / Neuroinflammatory
                      Diseases: genetics / Neuroinflammatory Diseases: pathology /
                      Humans / Microglia: metabolism / Mice, Transgenic / Mice,
                      Inbred C57BL / Alzheimer Disease: metabolism / Alzheimer
                      Disease: pathology / Alzheimer Disease: genetics / Membrane
                      Glycoproteins: metabolism / Membrane Glycoproteins: genetics
                      / Cells, Cultured / Male / Alzheimer’s disease (Other) /
                      Cytokine expression (Other) / MicroRNA (Other) / Microglia
                      (Other) / Neuroinflammation (Other) / Toll-like receptors
                      (Other) / MicroRNAs (NLM Chemicals) / Toll-Like Receptor 7
                      (NLM Chemicals) / Tlr7 protein, mouse (NLM Chemicals) /
                      MIRN29 microRNA, mouse (NLM Chemicals) / Membrane
                      Glycoproteins (NLM Chemicals) / MIRN29a microRNA, human (NLM
                      Chemicals)},
      cin          = {AG Wegmann / AG Heppner},
      ddc          = {610},
      cid          = {I:(DE-2719)1810006 / I:(DE-2719)1810007},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41514337},
      pmc          = {pmc:PMC12849500},
      doi          = {10.1186/s12974-025-03680-4},
      url          = {https://pub.dzne.de/record/284348},
}