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@ARTICLE{Kedia:271134,
      author       = {Kedia, Shreeya and Ji, Hao and Feng, Ruoqing and Androvic,
                      Peter and Spieth, Lena and Liu, Lu and Franz, Jonas and
                      Zdiarstek, Hanna and Anderson, Katrin Perez and Kaboglu, Cem
                      Busra and Liu, Qian and Mattugini, Nicola and Cherif, Fatma
                      and Prtvar, Danilo and Cantuti-Castelvetri, Ludovico and
                      Liesz, Arthur and Schifferer, Martina and Stadelmann,
                      Christine and Tahirovic, Sabina and Gokce, Ozgun and Simons,
                      Mikael},
      title        = {{T} cell-mediated microglial activation triggers myelin
                      pathology in a mouse model of amyloidosis.},
      journal      = {Nature neuroscience},
      volume       = {27},
      number       = {8},
      issn         = {1097-6256},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2024-01002},
      pages        = {1468 - 1474},
      year         = {2024},
      abstract     = {Age-related myelin damage induces inflammatory responses,
                      yet its involvement in Alzheimer's disease remains
                      uncertain, despite age being a major risk factor. Using a
                      mouse model of Alzheimer's disease, we found that
                      amyloidosis itself triggers age-related oligodendrocyte and
                      myelin damage. Mechanistically, CD8+ T cells promote the
                      progressive accumulation of abnormally interferon-activated
                      microglia that display myelin-damaging activity. Thus, our
                      data suggest that immune responses against myelinating
                      oligodendrocytes may contribute to neurodegenerative
                      diseases with amyloidosis.},
      keywords     = {Animals / Microglia: pathology / Microglia: metabolism /
                      Microglia: immunology / Myelin Sheath: pathology / Myelin
                      Sheath: metabolism / Mice / Disease Models, Animal /
                      Amyloidosis: pathology / Alzheimer Disease: pathology /
                      Alzheimer Disease: metabolism / Alzheimer Disease:
                      immunology / CD8-Positive T-Lymphocytes: immunology / Mice,
                      Transgenic / Oligodendroglia: pathology / Oligodendroglia:
                      metabolism / Mice, Inbred C57BL},
      cin          = {AG Simons / AG Tahirovic / AG Misgeld / AG Gokce},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008 / I:(DE-2719)1140003 /
                      I:(DE-2719)1110000-4 / I:(DE-2719)1013041},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11303250},
      pubmed       = {pmid:38937583},
      doi          = {10.1038/s41593-024-01682-8},
      url          = {https://pub.dzne.de/record/271134},
}