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@ARTICLE{Ying:258764,
      author       = {Ying, Johnson and Reboreda, Antonio and Yoshida, Motoharu
                      and Brandon, Mark P},
      title        = {{G}rid cell disruption in a mouse model of early
                      {A}lzheimer's disease reflects reduced integration of
                      self-motion cues.},
      journal      = {Current biology},
      volume       = {33},
      number       = {12},
      issn         = {0960-9822},
      address      = {London},
      publisher    = {Current Biology Ltd.},
      reportid     = {DZNE-2023-00672},
      pages        = {2425 - 2437.e5},
      year         = {2023},
      abstract     = {Converging evidence from human and rodent studies suggests
                      that disrupted grid cell coding in the medial entorhinal
                      cortex (MEC) underlies path integration behavioral deficits
                      during early Alzheimer's disease (AD). However, grid cell
                      firing relies on both self-motion cues and environmental
                      features, and it remains unclear whether disrupted grid
                      coding can account for specific path integration deficits
                      reported during early AD. Here, we report in the J20
                      transgenic amyloid beta (Aβ) mouse model of early AD that
                      grid cells were spatially unstable toward the center of the
                      arena, had qualitatively different spatial components that
                      aligned parallel to the borders of the environment, and
                      exhibited impaired integration of distance traveled via
                      reduced theta phase precession. Our results suggest that
                      disrupted early AD grid coding reflects reduced integration
                      of self-motion cues but not environmental information via
                      geometric boundaries, providing evidence that grid cell
                      impairments underlie path integration deficits during early
                      AD.},
      keywords     = {Humans / Mice / Animals / Cues / Alzheimer Disease:
                      genetics / Amyloid beta-Peptides / Mice, Transgenic /
                      Disease Models, Animal / Entorhinal Cortex / Action
                      Potentials / Alzheimer’s disease (Other) / Alzheimer’s
                      disease (Other) / Alzheimer’s disease (Other) /
                      Alzheimer’s disease (Other) / Fourier analysis (Other) /
                      amyloid beta (Other) / environmental geometry (Other) / grid
                      cells (Other) / medial entorhinal cortex (Other) / path
                      integration (Other) / spatial navigation (Other) / spatial
                      stability (Other) / theta phase precession (Other) / Amyloid
                      beta-Peptides (NLM Chemicals)},
      cin          = {AG Yoshida},
      ddc          = {570},
      cid          = {I:(DE-2719)1310011},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37220744},
      doi          = {10.1016/j.cub.2023.04.065},
      url          = {https://pub.dzne.de/record/258764},
}