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@ARTICLE{Varvel:138286,
      author       = {Varvel, Nicholas H and Grathwohl, Stefan A and Degenhardt,
                      Karoline and Resch, Claudia and Bosch, Andrea and Jucker,
                      Mathias and Neher, Jonas J},
      title        = {{R}eplacement of brain-resident myeloid cells does not
                      alter cerebral amyloid-β deposition in mouse models of
                      {A}lzheimer's disease.},
      journal      = {Journal of experimental medicine},
      volume       = {212},
      number       = {11},
      issn         = {1540-9538},
      address      = {New York, NY},
      publisher    = {Rockefeller Univ. Press},
      reportid     = {DZNE-2020-04608},
      pages        = {1803-1809},
      year         = {2015},
      abstract     = {Immune cells of myeloid lineage are encountered in the
                      Alzheimer's disease (AD) brain, where they cluster around
                      amyloid-β plaques. However, assigning functional roles to
                      myeloid cell subtypes has been problematic, and the
                      potential for peripheral myeloid cells to alleviate AD
                      pathology remains unclear. Therefore, we asked whether
                      replacement of brain-resident myeloid cells with peripheral
                      monocytes alters amyloid deposition in two mouse models of
                      cerebral β-amyloidosis (APP23 and APPPS1). Interestingly,
                      early after repopulation, infiltrating monocytes neither
                      clustered around plaques nor showed Trem2 expression.
                      However, with increasing time in the brain, infiltrating
                      monocytes became plaque associated and also Trem2 positive.
                      Strikingly, however, monocyte repopulation for up to 6 mo
                      did not modify amyloid load in either model, independent of
                      the stage of pathology at the time of repopulation. Our
                      results argue against a long-term role of peripheral
                      monocytes that is sufficiently distinct from microglial
                      function to modify cerebral β-amyloidosis. Therefore,
                      myeloid replacement by itself is not likely to be effective
                      as a therapeutic approach for AD.},
      keywords     = {Alzheimer Disease: metabolism / Alzheimer Disease:
                      pathology / Alzheimer Disease: therapy / Amyloid
                      beta-Peptides: metabolism / Animals / Brain: metabolism /
                      Brain: pathology / Disease Models, Animal / Female / Male /
                      Membrane Glycoproteins: analysis / Mice / Mice, Inbred C57BL
                      / Monocytes: physiology / Myeloid Cells: physiology /
                      Receptors, Immunologic: analysis / Amyloid beta-Peptides
                      (NLM Chemicals) / Membrane Glycoproteins (NLM Chemicals) /
                      Receptors, Immunologic (NLM Chemicals) / Trem2 protein,
                      mouse (NLM Chemicals)},
      cin          = {AG Jucker / AG Neher},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1210012},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26458770},
      pmc          = {pmc:PMC4612086},
      doi          = {10.1084/jem.20150478},
      url          = {https://pub.dzne.de/record/138286},
}