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@ARTICLE{Feiten:285462,
      author       = {Feiten, Astrid Feentje and Dahm, Kilian and Schlepckow, Kai
                      and van Lengerich, Bettina and Suh, Jung H and
                      Reifschneider, Anika and Wefers, Benedikt and Bartos, Laura
                      M and Wind, Karin and de Weerd, Lis and Ulas, Thomas and
                      De-Domenico, Elena and Grundschöttel, Pia and Paulusch,
                      Stefan and Tast, Benjamin and Honda, Tamisa and Müller,
                      Stephan A and Becker, Matthias and Khalin, Igor and Ricci,
                      Alessio and Liesz, Arthur and Brunner, Bettina and Krenner,
                      Claudia and Buschmann, Katrin and Nuscher, Brigitte and
                      Spieth, Lena and Junker, Niklas and Berghoff, Stefan A and
                      Davis, Sonnet S and Neher, Jonas J and Wurst, Wolfgang and
                      Plesnila, Nikolaus and Lewcock, Joseph W and Simons, Mikael
                      and Lichtenthaler, Stefan F and Di Paolo, Gilbert and
                      Brendel, Matthias and Capell, Anja and Monroe, Kathryn M and
                      Schultze, Joachim L and Haass, Christian},
      title        = {{TREM}2 expression level is critical for microglial state,
                      metabolic capacity and efficacy of {TREM}2 agonism.},
      journal      = {Nature Communications},
      volume       = {17},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2026-00240},
      pages        = {2002},
      year         = {2026},
      abstract     = {Triggering receptor expressed on myeloid cells 2 (TREM2) is
                      a central regulator of microglial activity and
                      loss-of-function coding variants are major risk factors for
                      late onset Alzheimer's disease (LOAD). To better understand
                      the molecular and functional changes associated with TREM2
                      signalling in microglia, we generated a TREM2 reporter
                      mouse. In APP transgenic animals, bulk RNA-sequencing of
                      isolated microglia sorted based on reporter expression
                      highlighted TREM2 level-related changes in major
                      immunometabolic pathways, and enrichment of genes in
                      oxidative phosphorylation and cholesterol metabolism in
                      microglia with increased TREM2 expression. Metabolic and
                      lipidomic profiling of sorted microglia showed that,
                      independent of Aβ pathology, TREM2 expression correlated
                      with signatures consistent with increased cellular redox,
                      energetics, and cholesterol homoeostasis. In accordance,
                      metabolic activity correlated with phagocytic capacity.
                      Finally, we performed chronic treatment with a TREM2 agonist
                      antibody and identified a window of TREM2 expression where
                      microglia are most responsive, thereby informing clinical
                      applications of TREM2 agonists.},
      cin          = {AG Haass / AG Schultze / AG Lichtenthaler / AG Becker / AG
                      Neher (München) / AG Simons / AG Wurst / PRECISE},
      ddc          = {500},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)1013038 /
                      I:(DE-2719)1110006 / I:(DE-2719)5000079 / I:(DE-2719)1110011
                      / I:(DE-2719)1110008 / I:(DE-2719)1140001 /
                      I:(DE-2719)1013031},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 354 - Disease
                      Prevention and Healthy Aging (POF4-354) / 351 - Brain
                      Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-351},
      experiment   = {EXP:(DE-2719)PRECISE-20190321},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41580393},
      pmc          = {pmc:PMC12936096},
      doi          = {10.1038/s41467-026-68706-8},
      url          = {https://pub.dzne.de/record/285462},
}