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@ARTICLE{Arbaciauskaite:285256,
      author       = {Arbaciauskaite, Skaiste and Silvestri, Simona and Luo,
                      Pingyan and Krüger, Christina and Mossmann, Zoe Julia and
                      Allelein, Susann and Scholz, Alexander and Loeffler, Dennis
                      and Fiorenza, Samuele and Menale, Anna and Torino, Enza and
                      Kuhlmeier, Dirk and Peters, Oliver and Lehnardt, Seija},
      title        = {{M}icroglia-{D}erived {E}xtracellular {V}esicles from
                      {A}lzheimer's {D}isease {P}atients {C}arry mi{RNA}s
                      {D}riving a {N}euroinflammatory {R}esponse.},
      journal      = {Molecular neurobiology},
      volume       = {63},
      number       = {1},
      issn         = {0893-7648},
      address      = {Totowa, NJ},
      publisher    = {Humana Press},
      reportid     = {DZNE-2026-00198},
      pages        = {435},
      year         = {2026},
      abstract     = {Alzheimer's disease (AD) represents the most common cause
                      of dementia and urgently requires sensitive biomarkers and
                      effective therapies. Extracellular vesicles represent
                      membranous nano-sized particles secreted from cells, which
                      serve as intercellular messengers participating in central
                      nervous system (CNS) homeostasis, but also are implicated in
                      AD pathogenesis. In addition, EVs containing
                      disease-specific signatures, such as microRNAs (miRNAs), are
                      considered as potent tools for the diagnosis and treatment
                      of AD and other brain disorders. In this study, we used
                      TMEM119 antibody to immunocapture microglia-derived EVs from
                      cerebrospinal fluid (CSF) of AD patients and control
                      subjects. EVs harvested from these CSF samples contained
                      distinct disease-specific miRNA profiles, as assessed by
                      small RNA sequencing. Using a HEK TLR reporter cell system,
                      we found that these miRNA are potent activators of human
                      TLR8, an established RNA sensor. Out of the miRNAs present
                      in AD-associated EVs, selected oligonucleotides were
                      synthesized and loaded into BV2 microglia-derived EVs.
                      Exposure of primary murine microglia to these miRNA-loaded
                      EVs led to TNF release from these cells, thereby driving a
                      neuroinflammatory response. Taken together, putatively
                      microglia-derived EVs from the CSF of AD patients contain
                      miRNAs, which are capable of activating hTLR8 and inducing
                      an inflammatory response from microglia.},
      keywords     = {Microglia: metabolism / Microglia: pathology / Alzheimer
                      Disease: genetics / Alzheimer Disease: cerebrospinal fluid /
                      Alzheimer Disease: pathology / Alzheimer Disease: metabolism
                      / Extracellular Vesicles: metabolism / Humans / MicroRNAs:
                      metabolism / MicroRNAs: genetics / Animals / Mice /
                      Neuroinflammatory Diseases: genetics / Neuroinflammatory
                      Diseases: pathology / Neuroinflammatory Diseases: metabolism
                      / Aged / Male / Female / HEK293 Cells / Aged, 80 and over /
                      Alzheimer’s disease (Other) / EV engineering (Other) /
                      Extracellular vesicles (Other) / MicroRNA (Other) /
                      Microglia (Other) / RNA delivery (Other) / Toll-like
                      Receptors (Other) / MicroRNAs (NLM Chemicals)},
      cin          = {AG Peters},
      ddc          = {570},
      cid          = {I:(DE-2719)5000000},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41678018},
      pmc          = {pmc:PMC12901236},
      doi          = {10.1007/s12035-026-05719-w},
      url          = {https://pub.dzne.de/record/285256},
}