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@ARTICLE{Keane:153985,
      author       = {Keane, Lily and Antignano, Ignazio and Riechers,
                      Sean-Patrick and Zollinger, Raphael and Dumas, Anaelle A.
                      and Offermann, Nina and Bernis, Maria E. and Russ, Jenny and
                      Graelmann, Frederike and McCormick, Patrick Neil and Esser,
                      Julia and Tejera, Dario and Nagano, Ai and Wang, Jun and
                      Chelala, Claude and Biederbick, Yvonne and Halle, Annett and
                      Salomoni, Paolo and Heneka, Michael T. and Capasso, Melania},
      title        = {m{TOR}-dependent translation amplifies microglia priming in
                      aging mice},
      journal      = {The journal of clinical investigation},
      volume       = {131},
      number       = {1},
      issn         = {1558-8238},
      address      = {Ann Arbor, Mich.},
      publisher    = {ASCJ},
      reportid     = {DZNE-2021-00002},
      pages        = {e132727},
      year         = {2021},
      abstract     = {Microglia maintain homeostasis in the brain. However, with
                      age, they become primed and respond more strongly to
                      inflammatory stimuli. We show here that microglia from aged
                      mice had upregulated mTOR complex 1 signaling controlling
                      translation, as well as protein levels of inflammatory
                      mediators. Genetic ablation of mTOR signaling showed a dual
                      yet contrasting effect on microglia priming: it caused an
                      NF-κB–dependent upregulation of priming genes at the mRNA
                      level; however, mice displayed reduced cytokine protein
                      levels, diminished microglia activation, and milder sickness
                      behavior. The effect on translation was dependent on reduced
                      phosphorylation of 4EBP1, resulting in decreased binding of
                      eIF4E to eIF4G. Similar changes were present in aged human
                      microglia and in damage-associated microglia, indicating
                      that upregulation of mTOR-dependent translation is an
                      essential aspect of microglia priming in aging and
                      neurodegeneration.},
      keywords     = {Aging: genetics / Aging: metabolism / Animals / Eukaryotic
                      Initiation Factor-4E: genetics / Eukaryotic Initiation
                      Factor-4E: metabolism / Eukaryotic Initiation Factor-4G:
                      genetics / Eukaryotic Initiation Factor-4G: metabolism /
                      Humans / Mice / Mice, Transgenic / Microglia: enzymology /
                      NF-kappa B: genetics / NF-kappa B: metabolism /
                      Phosphorylation: genetics / Protein Biosynthesis / Signal
                      Transduction / TOR Serine-Threonine Kinases: genetics / TOR
                      Serine-Threonine Kinases: metabolism},
      cin          = {AG Capasso / AG Heneka ; AG Heneka / AG Salomoni / AG
                      Halle},
      ddc          = {610},
      cid          = {I:(DE-2719)1013033 / I:(DE-2719)1011303 /
                      I:(DE-2719)1013032 / I:(DE-2719)1013034},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352) / 353 - Clinical and Health Care Research
                      (POF4-353)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352 /
                      G:(DE-HGF)POF4-353},
      experiment   = {EXP:(DE-2719)IDAF-20190308 / EXP:(DE-2719)LMF-20190308},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC7773382},
      pubmed       = {pmid:33108356},
      doi          = {10.1172/JCI132727},
      url          = {https://pub.dzne.de/record/153985},
}