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@ARTICLE{VianadaSilva:266787,
      author       = {Viana-da-Silva, Silvia and Haberl, Matthias and Gaur,
                      Kshitij and Patel, Rina and Narayan, Gautam and Ledakis, Max
                      and Fu, Maylin L and de Castro Vieira, Miguel and Koo,
                      Edward H and Leutgeb, Jill K and Leutgeb, Stefan},
      title        = {{L}ocalized {APP} expression results in progressive network
                      dysfunction by disorganizing spike timing.},
      journal      = {Neuron},
      volume       = {112},
      number       = {1},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2024-00045},
      pages        = {124 - 140.e6},
      year         = {2024},
      abstract     = {Progressive cognitive decline in Alzheimer's disease could
                      either be caused by a spreading molecular pathology or by an
                      initially focal pathology that causes aberrant neuronal
                      activity in a larger network. To distinguish between these
                      possibilities, we generated a mouse model with expression of
                      mutant human amyloid precursor protein (APP) in only
                      hippocampal CA3 cells. We found that performance in a
                      hippocampus-dependent memory task was impaired in young
                      adult and aged mutant mice. In both age groups, we then
                      recorded from the CA1 region, which receives inputs from
                      APP-expressing CA3 cells. We observed that theta oscillation
                      frequency in CA1 was reduced along with disrupted relative
                      timing of principal cells. Highly localized pathology
                      limited to the presynaptic CA3 cells is thus sufficient to
                      cause aberrant firing patterns in postsynaptic neuronal
                      networks, which indicates that disease progression is not
                      only from spreading pathology but also mediated by
                      progressively advancing physiological dysfunction.},
      keywords     = {Mice / Humans / Animals / Aged / Amyloid beta-Protein
                      Precursor: genetics / Amyloid beta-Protein Precursor:
                      metabolism / Hippocampus: metabolism / Neurons: physiology /
                      Alzheimer Disease: metabolism / Synapses: physiology / Mice,
                      Transgenic / Alzheimer’s disease (Other) / Alzheimer’s
                      disease (Other) / Alzheimer’s disease (Other) /
                      Alzheimer’s disease (Other) / Alzheimer’s disease
                      (Other) / Alzheimer’s disease (Other) / amyloid precursor
                      protein (Other) / hippocampus (Other) / phase precession
                      (Other) / spike timing (Other) / theta oscillations (Other)
                      / Amyloid beta-Protein Precursor (NLM Chemicals)},
      cin          = {AG Viana-da-Silva},
      ddc          = {610},
      cid          = {I:(DE-2719)5000068},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10877582},
      pubmed       = {pmid:37909036},
      doi          = {10.1016/j.neuron.2023.10.001},
      url          = {https://pub.dzne.de/record/266787},
}