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@ARTICLE{McNamara:169135,
      author       = {McNamara, Niamh B and Munro, David A D and Bestard-Cuche,
                      Nadine and Uyeda, Akiko and Bogie, Jeroen F J and Hoffmann,
                      Alana and Holloway, Rebecca K and Molina-Gonzalez, Irene and
                      Askew, Katharine E and Mitchell, Stephen and Mungall,
                      William and Dodds, Michael and Dittmayer, Carsten and Moss,
                      Jonathan and Rose, Jamie and Szymkowiak, Stefan and Amann,
                      Lukas and McColl, Barry W and Prinz, Marco and Spires-Jones,
                      Tara L and Stenzel, Werner and Horsburgh, Karen and
                      Hendriks, Jerome J A and Pridans, Clare and Muramatsu, Rieko
                      and Williams, Anna and Priller, Josef and Miron, Veronique
                      E},
      title        = {{M}icroglia regulate central nervous system myelin growth
                      and integrity.},
      journal      = {Nature},
      volume       = {613},
      number       = {7942},
      issn         = {0028-0836},
      address      = {London [u.a.]},
      publisher    = {Nature Publ. Group},
      reportid     = {DZNE-2023-00014},
      pages        = {120 - 129},
      year         = {2023},
      abstract     = {Myelin is required for the function of neuronal axons in
                      the central nervous system, but the mechanisms that support
                      myelin health are unclear. Although macrophages in the
                      central nervous system have been implicated in myelin
                      health1, it is unknown which macrophage populations are
                      involved and which aspects they influence. Here we show that
                      resident microglia are crucial for the maintenance of myelin
                      health in adulthood in both mice and humans. We demonstrate
                      that microglia are dispensable for developmental myelin
                      ensheathment. However, they are required for subsequent
                      regulation of myelin growth and associated cognitive
                      function, and for preservation of myelin integrity by
                      preventing its degeneration. We show that loss of myelin
                      health due to the absence of microglia is associated with
                      the appearance of a myelinating oligodendrocyte state with
                      altered lipid metabolism. Moreover, this mechanism is
                      regulated through disruption of the TGFβ1-TGFβR1 axis. Our
                      findings highlight microglia as promising therapeutic
                      targets for conditions in which myelin growth and integrity
                      are dysregulated, such as in ageing and neurodegenerative
                      disease2,3.},
      keywords     = {Central Nervous System: cytology / Humans / Mice / Animals
                      / Adult / Myelin Sheath: metabolism / Microglia: metabolism
                      / Neurodegenerative Diseases: metabolism / Central Nervous
                      System: metabolism / Axons: metabolism / Oligodendroglia /
                      Central Nervous System: pathology / Microglia: cytology /
                      Microglia: pathology / Myelin Sheath: pathology /
                      Neurodegenerative Diseases: pathology / Oligodendroglia:
                      metabolism / Oligodendroglia: pathology / Cognition /
                      Transforming Growth Factor beta1: metabolism / Receptor,
                      Transforming Growth Factor-beta Type I: metabolism / Lipid
                      Metabolism / Aging: metabolism / Aging: pathology /
                      Transforming Growth Factor beta1 (NLM Chemicals) / Receptor,
                      Transforming Growth Factor-beta Type I (NLM Chemicals)},
      cin          = {Clinical Study Team Berlin 1},
      ddc          = {500},
      cid          = {I:(DE-2719)5000007},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9812791},
      pubmed       = {pmid:36517604},
      doi          = {10.1038/s41586-022-05534-y},
      url          = {https://pub.dzne.de/record/169135},
}