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@ARTICLE{Parhizkar:140448,
      author       = {Parhizkar, Samira and Arzberger, Thomas and Brendel,
                      Matthias and Kleinberger, Gernot and Deussing, Maximilian
                      and Focke, Carola and Nuscher, Brigitte and Xiong, Monica
                      and Ghasemigharagoz, Alireza and Katzmarski, Natalie and
                      Krasemann, Susanne and Lichtenthaler, Stefan F and Müller,
                      Stephan A and Colombo, Alessio and Sebastian Monasor, Laura
                      and Tahirovic, Sabina and Herms, Jochen and Willem, Michael
                      and Pettkus, Nadine and Butovsky, Oleg and Bartenstein,
                      Peter and Edbauer, Dieter and Rominger, Axel and Ertürk,
                      Ali and Grathwohl, Stefan A and Neher, Jonas J and Holtzman,
                      David M and Meyer-Luehmann, Melanie and Haass, Christian},
      title        = {{L}oss of {TREM}2 function increases amyloid seeding but
                      reduces plaque-associated {A}po{E}.},
      journal      = {Nature reviews / Neuroscience},
      volume       = {22},
      number       = {2},
      issn         = {1097-6256},
      address      = {London},
      publisher    = {Nature Publ. Group58142},
      reportid     = {DZNE-2020-06770},
      pages        = {191-204},
      year         = {2019},
      abstract     = {Coding variants in the triggering receptor expressed on
                      myeloid cells 2 (TREM2) are associated with late-onset
                      Alzheimer's disease (AD). We demonstrate that amyloid plaque
                      seeding is increased in the absence of functional Trem2.
                      Increased seeding is accompanied by decreased microglial
                      clustering around newly seeded plaques and reduced
                      plaque-associated apolipoprotein E (ApoE). Reduced ApoE
                      deposition in plaques is also observed in brains of AD
                      patients carrying TREM2 coding variants. Proteomic analyses
                      and microglia depletion experiments revealed microglia as
                      one origin of plaque-associated ApoE. Longitudinal amyloid
                      small animal positron emission tomography demonstrates
                      accelerated amyloidogenesis in Trem2 loss-of-function
                      mutants at early stages, which progressed at a lower rate
                      with aging. These findings suggest that in the absence of
                      functional Trem2, early amyloidogenesis is accelerated due
                      to reduced phagocytic clearance of amyloid seeds despite
                      reduced plaque-associated ApoE.},
      keywords     = {Alzheimer Disease: genetics / Alzheimer Disease: metabolism
                      / Alzheimer Disease: pathology / Amyloid: metabolism /
                      Amyloid beta-Peptides: genetics / Amyloid beta-Peptides:
                      metabolism / Amyloid beta-Protein Precursor: genetics /
                      Amyloid beta-Protein Precursor: metabolism / Animals /
                      Apolipoproteins E: metabolism / Brain: metabolism / Brain:
                      pathology / Disease Models, Animal / Genotype / Humans /
                      Membrane Glycoproteins: genetics / Membrane Glycoproteins:
                      metabolism / Mice / Mice, Transgenic / Microglia: metabolism
                      / Microglia: pathology / Phagocytosis: physiology / Plaque,
                      Amyloid: genetics / Plaque, Amyloid: metabolism / Plaque,
                      Amyloid: pathology / Receptors, Immunologic: genetics /
                      Receptors, Immunologic: metabolism / Amyloid (NLM Chemicals)
                      / Amyloid beta-Peptides (NLM Chemicals) / Amyloid
                      beta-Protein Precursor (NLM Chemicals) / Apolipoproteins E
                      (NLM Chemicals) / Membrane Glycoproteins (NLM Chemicals) /
                      Receptors, Immunologic (NLM Chemicals) / Trem2 protein,
                      mouse (NLM Chemicals)},
      cin          = {AG Levin / AG Lichtenthaler / AG Tahirovic / AG Herms / AG
                      Haass / AG Neher (Tübingen) / AG Edbauer},
      ddc          = {570},
      cid          = {I:(DE-2719)1111016 / I:(DE-2719)1110006 /
                      I:(DE-2719)1140003 / I:(DE-2719)1110001 / I:(DE-2719)1110007
                      / I:(DE-2719)1210012 / I:(DE-2719)1110004},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30617257},
      pmc          = {pmc:PMC6417433},
      doi          = {10.1038/s41593-018-0296-9},
      url          = {https://pub.dzne.de/record/140448},
}