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@ARTICLE{Safaiyani:157763,
      author       = {Safaiyani, Shima and Besson-Girard, Simon and Kaya,
                      Tuğberk and Cantuti-Castelvetri, Ludovico and Liu, Lu and
                      Ji, Hao and Schifferer, Martina and Gouna, Garyfallia and
                      Usifo, Fumere and Kannaiyan, Nirmal and Fitzner, Dirk and
                      Xiang, Xianyuan and Rossner, Moritz J and Brendel, Matthias
                      and Gökce, Ozgun and Simons, Mikael},
      title        = {{W}hite matter aging drives microglial diversity.},
      journal      = {Neuron},
      volume       = {109},
      number       = {7},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2021-01220},
      pages        = {1100 - 1117.e10},
      year         = {2021},
      abstract     = {Aging results in gray and white matter degeneration, but
                      the specific microglial responses are unknown. Using
                      single-cell RNA sequencing from white and gray matter
                      separately, we identified white matter-associated microglia
                      (WAMs), which share parts of the disease-associated
                      microglia (DAM) gene signature and are characterized by
                      activation of genes implicated in phagocytic activity and
                      lipid metabolism. WAMs depend on triggering receptor
                      expressed on myeloid cells 2 (TREM2) signaling and are aging
                      dependent. In the aged brain, WAMs form independent of
                      apolipoprotein E (APOE), in contrast to mouse models of
                      Alzheimer's disease, in which microglia with the WAM gene
                      signature are generated prematurely and in an APOE-dependent
                      pathway similar to DAMs. Within the white matter, microglia
                      frequently cluster in nodules, where they are engaged in
                      clearing degenerated myelin. Thus, WAMs may represent a
                      potentially protective response required to clear
                      degenerated myelin accumulating during white matter aging
                      and disease.},
      keywords     = {Aging: physiology / Alzheimer Disease: genetics / Animals /
                      Apolipoproteins E: genetics / Demyelinating Diseases:
                      pathology / Gene Expression Regulation / Gray Matter:
                      cytology / Gray Matter: growth $\&$ development /
                      Immunohistochemistry / Membrane Glycoproteins: biosynthesis
                      / Membrane Glycoproteins: genetics / Mice / Mice, Inbred
                      C57BL / Mice, Knockout / Microglia: physiology / Microglia:
                      ultrastructure / Myelin Sheath: metabolism / Receptors,
                      Immunologic: biosynthesis / Receptors, Immunologic: genetics
                      / Sequence Analysis, RNA / Signal Transduction: physiology /
                      Single-Cell Analysis / White Matter: cytology / White
                      Matter: growth $\&$ development / ApoE (Other) / Trem2
                      (Other) / microglia, aging (Other) / myelin (Other) / white
                      matter (Other) / Apolipoproteins E (NLM Chemicals) /
                      Membrane Glycoproteins (NLM Chemicals) / Receptors,
                      Immunologic (NLM Chemicals) / Trem2 protein, mouse (NLM
                      Chemicals)},
      cin          = {AG Simons / AG Misgeld},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008 / I:(DE-2719)1110000-4},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33606969},
      doi          = {10.1016/j.neuron.2021.01.027},
      url          = {https://pub.dzne.de/record/157763},
}