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@ARTICLE{Groh:279051,
      author       = {Groh, Janos and Feng, Ruoqing and Yuan, Xidi and Liu, Lu
                      and Klein, Dennis and Hutahaean, Gladis and Butz, Elisabeth
                      and Wang, Zhen and Steinbrecher, Lisa and Neher, Jonas and
                      Martini, Rudolf and Simons, Mikael},
      title        = {{M}icroglia activation orchestrates {CXCL}10-mediated
                      {CD}8+ {T} cell recruitment to promote aging-related white
                      matter degeneration.},
      journal      = {Nature neuroscience},
      volume       = {28},
      number       = {6},
      issn         = {1097-6256},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2025-00681},
      pages        = {1160 - 1173},
      year         = {2025},
      abstract     = {Aging is the major risk factor for neurodegeneration and is
                      associated with structural and functional alterations in
                      white matter. Myelin is particularly vulnerable to aging,
                      resulting in white matter-associated microglia activation.
                      Here we used pharmacological and genetic approaches to
                      investigate microglial functions related to aging-associated
                      changes in myelinated axons of mice. Our results reveal that
                      maladaptive microglia activation promotes the accumulation
                      of harmful CD8+ T cells, leading to the degeneration of
                      myelinated axons and subsequent impairment of brain function
                      and behavior. We characterize glial heterogeneity and
                      aging-related changes in white matter by single-cell and
                      spatial transcriptomics and reveal elaborate glial-immune
                      interactions. Mechanistically, we show that the CXCL10-CXCR3
                      axis is crucial for the recruitment and retention of CD8+ T
                      cells in aged white matter, where they exert pathogenic
                      effects. Our results indicate that myelin-related microglia
                      dysfunction promotes adaptive immune reactions in aging and
                      identify putative targets to mitigate their detrimental
                      impact.},
      keywords     = {Animals / Microglia: immunology / Microglia: metabolism /
                      White Matter: pathology / White Matter: immunology / White
                      Matter: metabolism / CD8-Positive T-Lymphocytes: immunology
                      / CD8-Positive T-Lymphocytes: metabolism / Mice / Aging:
                      pathology / Aging: immunology / Chemokine CXCL10: metabolism
                      / Chemokine CXCL10: immunology / Mice, Inbred C57BL /
                      Receptors, CXCR3: metabolism / Myelin Sheath / Male / Mice,
                      Transgenic / Nerve Degeneration: pathology / Nerve
                      Degeneration: immunology / Chemokine CXCL10 (NLM Chemicals)
                      / Receptors, CXCR3 (NLM Chemicals) / Cxcl10 protein, mouse
                      (NLM Chemicals) / Cxcr3 protein, mouse (NLM Chemicals)},
      cin          = {AG Simons / AG Neher (München) / AG Neher (Tübingen)},
      ddc          = {610},
      cid          = {I:(DE-2719)1110008 / I:(DE-2719)1110011 /
                      I:(DE-2719)1210012},
      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},
      pubmed       = {pmid:40404995},
      doi          = {10.1038/s41593-025-01955-w},
      url          = {https://pub.dzne.de/record/279051},
}