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@ARTICLE{Poll:153300,
      author       = {Poll, Stefanie and Mittag, Manuel and Musacchio, Fabrizio
                      and Justus, Lena C and Giovannetti, Eleonora Ambrad and
                      Steffen, Julia and Wagner, Jens and Zohren, Lioba and
                      Schoch, Susanne and Schmidt, Boris and Jackson, Walker S and
                      Ehninger, Dan and Fuhrmann, Martin},
      title        = {{M}emory trace interference impairs recall in a mouse model
                      of {A}lzheimer's disease.},
      journal      = {Nature neuroscience},
      volume       = {23},
      number       = {8},
      issn         = {1546-1726},
      address      = {New York, NY},
      publisher    = {Nature America},
      reportid     = {DZNE-2020-01297},
      pages        = {952 - 958},
      year         = {2020},
      abstract     = {In Alzheimer's disease (AD), hippocampus-dependent memories
                      underlie an extensive decline. The neuronal ensemble
                      encoding a memory, termed engram, is partially recapitulated
                      during memory recall. Artificial activation of an engram can
                      restore memory in a mouse model of early AD, but its fate
                      and the factors that render the engram nonfunctional are yet
                      to be revealed. Here, we used repeated two-photon in vivo
                      imaging to analyze fosGFP transgenic mice (which express
                      enhanced GFP under the Fos promoter) performing a
                      hippocampus-dependent memory task. We found that partial
                      reactivation of the CA1 engram during recall is preserved
                      under AD-like conditions. However, we identified a
                      novelty-like ensemble that interfered with the engram and
                      thus compromised recall. Mimicking a novelty-like ensemble
                      in healthy mice was sufficient to affect memory recall. In
                      turn, reducing the novelty-like signal rescued the recall
                      impairment under AD-like conditions. These findings suggest
                      a novel mechanistic process that contributes to the
                      deterioration of memories in AD.},
      keywords     = {Alzheimer Disease: genetics / Alzheimer Disease: metabolism
                      / Alzheimer Disease: physiopathology / Amyloid beta-Protein
                      Precursor: genetics / Amyloid beta-Protein Precursor:
                      metabolism / Animals / Disease Models, Animal / Female /
                      Hippocampus: physiology / Male / Mental Recall: physiology /
                      Mice / Mice, Transgenic / Neurons: physiology / Optogenetics
                      / Proto-Oncogene Proteins c-fos: genetics / Proto-Oncogene
                      Proteins c-fos: metabolism / Amyloid beta-Protein Precursor
                      (NLM Chemicals) / Proto-Oncogene Proteins c-fos (NLM
                      Chemicals)},
      cin          = {AG Fuhrmann / AG Jackson / AG Ehninger},
      ddc          = {610},
      cid          = {I:(DE-2719)1011004 / I:(DE-2719)1013019 /
                      I:(DE-2719)1013005},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32514139},
      doi          = {10.1038/s41593-020-0652-4},
      url          = {https://pub.dzne.de/record/153300},
}