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@ARTICLE{Joshi:162686,
      author       = {Joshi, Pranav and Riffel, Florian and Kumar, Sathish and
                      Villacampa, Nàdia and Theil, Sandra and Parhizkar, Samira
                      and Haass, Christian and Colonna, Marco and Heneka, Michael
                      and Arzberger, Thomas and Herms, Jochen and Walter, Jochen},
      title        = {{TREM}2 modulates differential deposition of modified and
                      non-modified {A}β species in extracellular plaques and
                      intraneuronal deposits.},
      journal      = {Acta Neuropathologica Communications},
      volume       = {9},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2021-01343},
      pages        = {168},
      year         = {2021},
      note         = {CC BY},
      abstract     = {Progressive accumulation of Amyloid-β (Aβ) deposits in
                      the brain is a characteristic neuropathological hallmark of
                      Alzheimer's disease (AD). During disease progression,
                      extracellular Aβ plaques undergo specific changes in their
                      composition by the sequential deposition of different
                      modified Aβ species. Microglia are implicated in the
                      restriction of amyloid deposits and play a major role in
                      internalization and degradation of Aβ. Recent studies
                      showed that rare variants of the Triggering Receptor
                      Expressed on Myeloid cells 2 (TREM2) are associated with an
                      increased risk for AD. Post-translational modifications of
                      Aβ could modulate the interaction with TREM2, and the
                      uptake by microglia. Here, we demonstrate that genetic
                      deletion of TREM2 or expression of a disease associated
                      TREM2 variant in mice lead to differential accumulation of
                      modified and non-modified Aβ species in extracellular
                      plaques and intraneuronal deposits. Human brains with rare
                      TREM2 AD risk variants also showed altered deposition of
                      modified Aβ species in the different brain lesions as
                      compared to cases with the common variant of TREM2. These
                      findings indicate that TREM2 plays a critical role in the
                      development and the composition of Aβ deposits, not only in
                      extracellular plaques, but also intraneuronally, that both
                      could contribute to the pathogenesis of AD.},
      keywords     = {Aged / Aged, 80 and over / Alzheimer Disease: pathology /
                      Amyloid beta-Peptides: chemistry / Amyloid beta-Peptides:
                      metabolism / Animals / Female / Humans / Male / Membrane
                      Glycoproteins: genetics / Membrane Glycoproteins: metabolism
                      / Mice / Neurons: pathology / Plaque, Amyloid: chemistry /
                      Plaque, Amyloid: pathology / Receptors, Immunologic:
                      genetics / Receptors, Immunologic: metabolism / Aβ (Other)
                      / Intraneuronal (Other) / Microglia (Other) /
                      Post-translational modification (Other) / TREM2 (Other) /
                      Vascular deposits (Other)},
      cin          = {AG Haass / Biomarker / AG Herms / Neuropathology /
                      Brainbank},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007 / I:(DE-2719)1011301 /
                      I:(DE-2719)1110001 / I:(DE-2719)1140013},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34663480},
      pmc          = {pmc:PMC8522217},
      doi          = {10.1186/s40478-021-01263-x},
      url          = {https://pub.dzne.de/record/162686},
}