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@ARTICLE{Colas:139181,
      author       = {Colas, Damien and Chuluun, Bayarsaikhan and Garner, Craig C
                      and Heller, H Craig},
      title        = {{S}hort-term treatment with flumazenil restores long-term
                      object memory in a mouse model of {D}own syndrome.},
      journal      = {Neurobiology of learning and memory},
      volume       = {140},
      issn         = {1074-7427},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2020-05503},
      pages        = {11-16},
      year         = {2017},
      abstract     = {Down syndrome (DS) is a common genetic cause of
                      intellectual disability yet no pro-cognitive drug therapies
                      are approved for human use. Mechanistic studies in a mouse
                      model of DS (Ts65Dn mice) demonstrate that impaired
                      cognitive function is due to excessive neuronal inhibitory
                      tone. These deficits are normalized by chronic, short-term
                      low doses of GABAA receptor (GABAAR) antagonists in adult
                      animals, but none of the compounds investigated are approved
                      for human use. We explored the therapeutic potential of
                      flumazenil (FLUM), a GABAAR antagonist working at the
                      benzodiazepine binding site that has FDA approval. Long-term
                      memory was assessed by the Novel Object Recognition (NOR)
                      testing in Ts65Dn mice after acute or short-term chronic
                      treatment with FLUM. Short-term, low, chronic dose regimens
                      of FLUM elicit long-lasting (>1week) normalization of
                      cognitive function in both young and aged mice. FLUM at low
                      dosages produces long lasting cognitive improvements and has
                      the potential of fulfilling an unmet therapeutic need in
                      DS.},
      keywords     = {Animals / Cognition: drug effects / Disease Models, Animal
                      / Down Syndrome: drug therapy / Down Syndrome: genetics /
                      Flumazenil: pharmacology / Flumazenil: therapeutic use /
                      GABA Modulators: pharmacology / GABA Modulators: therapeutic
                      use / Male / Memory Disorders: drug therapy / Memory,
                      Long-Term: drug effects / Mice / GABA Modulators (NLM
                      Chemicals) / Flumazenil (NLM Chemicals)},
      cin          = {AG Garner},
      ddc          = {570},
      cid          = {I:(DE-2719)1810001},
      pnm          = {341 - Molecular Signaling (POF3-341)},
      pid          = {G:(DE-HGF)POF3-341},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28215510},
      doi          = {10.1016/j.nlm.2017.02.006},
      url          = {https://pub.dzne.de/record/139181},
}