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@MISC{Arnoux:169082,
      author       = {Arnoux, Isabelle and Willam, Michael and Griesche, Nadine
                      and Krummeich, Jennifer and Watari, Hirofumi and Offermann,
                      Nina and Weber, Stephanie and Narayan Dey, Partha and Chen,
                      Chen and Monteiro, Olivia and Buettner, Sven and Meyer,
                      Katharina and Bano, Daniele and Radyushkin, Konstantin and
                      Langston, Rosamund and Lambert, Jeremy J. and Wanker, Erich
                      and Methner, Axel and Krauss, Sybille and Schweiger, Susann
                      and Stroh, Albrecht},
      title        = {{D}ataset: {D}ata from: {M}etformin reverses early cortical
                      network dysfunction and behavior changes in {H}untington’s
                      disease},
      publisher    = {Dryad},
      reportid     = {DZNE-2022-01789},
      year         = {2018},
      abstract     = {Catching primal functional changes in early, “very far
                      from disease onset” (VFDO) stages of Huntington’s
                      disease is likely to be the key to a successful therapy.
                      Focusing on VFDO stages, we assessed neuronal microcircuits
                      in premanifest Hdh150 knock-in mice. Employing in vivo
                      two-photon Ca2+ imaging, we revealed an early pattern of
                      circuit dysregulation in the visual cortex- one of the first
                      regions affected in premanifest Huntington’s disease -
                      characterized by an increase in activity, an enhanced
                      synchronicity and hyperactive neurons. These findings are
                      accompanied by aberrations in animal behavior. We
                      furthermore show that the anti-diabetic drug metformin
                      diminishes aberrant Huntingtin protein load and fully
                      restores both, early network activity patterns and
                      behavioral aberrations. This network-centered approach
                      reveals a critical window of vulnerability far before
                      clinical manifestation and establishes metformin as a
                      promising candidate for a chronic therapy starting early in
                      premanifest Huntington’s disease pathogenesis long before
                      the onset of clinical symptoms.},
      keywords     = {cortical microcircuits (Other) / Huntington disease (Other)
                      / in vivo calcium imaging (Other) / metformin (Other) /
                      neuronal hyperactivity (Other)},
      cin          = {AG Krauß / AG Bano / AG Capasso / Biorepository},
      cid          = {I:(DE-2719)1011006 / I:(DE-2719)1013003 /
                      I:(DE-2719)1013033 / I:(DE-2719)1040300},
      pnm          = {351 - Brain Function (POF4-351) / 352 - Disease Mechanisms
                      (POF4-352)},
      pid          = {G:(DE-HGF)POF4-351 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)32},
      doi          = {10.5061/dryad.g3b5272},
      url          = {https://pub.dzne.de/record/169082},
}