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@ARTICLE{Uhlmann:154283,
      author       = {Uhlmann, Ruth E and Rother, Christine and Rasmussen, Jay
                      and Schelle, Juliane and Bergmann, Carina and Ullrich
                      Gavilanes, Emily M and Fritschi, Sarah and Buehler, Anika
                      and Baumann, Frank and Skodras, Angelos and Al-Shaana, Rawaa
                      and Beschorner, Natalie and Ye, Lan and Kaeser, Stephan A
                      and Obermüller, Ulrike and Christensen, Søren and
                      Kartberg, Fredrik and Stavenhagen, Jeffrey B and Rahfeld,
                      Jens-Ulrich and Cynis, Holger and Qian, Fang and Weinreb,
                      Paul H and Bussiere, Thierry and Walker, Lary C and
                      Staufenbiel, Matthias and Jucker, Mathias},
      title        = {{A}cute targeting of pre-amyloid seeds in transgenic mice
                      reduces {A}lzheimer-like pathology later in life.},
      journal      = {Nature neuroscience},
      volume       = {23},
      number       = {12},
      issn         = {1546-1726},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2021-00137},
      pages        = {1580 - 1588},
      year         = {2020},
      note         = {ISSN 1546-1726 not unique: **3 hits**.},
      abstract     = {Amyloid-β (Aβ) deposits are a relatively late consequence
                      of Aβ aggregation in Alzheimer's disease. When pathogenic
                      Aβ seeds begin to form, propagate and spread is not known,
                      nor are they biochemically defined. We tested various
                      antibodies for their ability to neutralize Aβ seeds before
                      Aβ deposition becomes detectable in Aβ precursor
                      protein-transgenic mice. We also characterized the different
                      antibody recognition profiles using immunoprecipitation of
                      size-fractionated, native, mouse and human brain-derived Aβ
                      assemblies. At least one antibody, aducanumab, after acute
                      administration at the pre-amyloid stage, led to a
                      significant reduction of Aβ deposition and downstream
                      pathologies 6 months later. This demonstrates that
                      therapeutically targetable pathogenic Aβ seeds already
                      exist during the lag phase of protein aggregation in the
                      brain. Thus, the preclinical phase of Alzheimer's
                      disease-currently defined as Aβ deposition without clinical
                      symptoms-may be a relatively late manifestation of a much
                      earlier pathogenic seed formation and propagation that
                      currently escapes detection in vivo.},
      keywords     = {Aged / Aged, 80 and over / Alzheimer Disease: metabolism /
                      Alzheimer Disease: pathology / Amyloid beta-Peptides:
                      metabolism / Amyloid beta-Protein Precursor: antagonists
                      $\&$ inhibitors / Animals / Antibodies, Blocking:
                      pharmacology / Antibodies, Monoclonal, Humanized:
                      pharmacokinetics / Antibodies, Monoclonal, Humanized:
                      pharmacology / Brain Chemistry / Humans / Male / Mice /
                      Mice, Inbred C57BL / Mice, Transgenic / Middle Aged /
                      Neurofilament Proteins: cerebrospinal fluid / Plaque,
                      Amyloid: pathology / Tissue Extracts: pharmacology / Amyloid
                      beta-Peptides (NLM Chemicals) / Amyloid beta-Protein
                      Precursor (NLM Chemicals) / Antibodies, Blocking (NLM
                      Chemicals) / Antibodies, Monoclonal, Humanized (NLM
                      Chemicals) / Neurofilament Proteins (NLM Chemicals) / Tissue
                      Extracts (NLM Chemicals) / aducanumab (NLM Chemicals)},
      cin          = {AG Jucker / Ext UKT},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)5000058},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33199898},
      pmc          = {pmc:PMC7783656},
      doi          = {10.1038/s41593-020-00737-w},
      url          = {https://pub.dzne.de/record/154283},
}