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@ARTICLE{Benito:139529,
      author       = {Benito, E. and Ramachandran, B. and Schroeder, H. and
                      Schmidt, G. and Urbanke, H. and Burkhardt, S. and Capece, V.
                      and Dean, C. and Fischer, A.},
      title        = {{T}he {BET}/{BRD} inhibitor {JQ}1 improves brain plasticity
                      in {WT} and {APP} mice.},
      journal      = {Translational Psychiatry},
      volume       = {7},
      number       = {9},
      issn         = {2158-3188},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DZNE-2020-05851},
      pages        = {e1239},
      year         = {2017},
      abstract     = {Histone acetylation is essential for memory formation and
                      its deregulation contributes to the pathogenesis of
                      Alzheimer's disease. Thus, targeting histone acetylation is
                      discussed as a novel approach to treat dementia. The histone
                      acetylation landscape is shaped by chromatin writer and
                      eraser proteins, while readers link chromatin state to
                      cellular function. Chromatin readers emerged novel drug
                      targets in cancer research but little is known about the
                      manipulation of readers in the adult brain. Here we tested
                      the effect of JQ1-a small-molecule inhibitor of the
                      chromatin readers BRD2, BRD3, BRD4 and BRDT-on brain
                      function and show that JQ1 is able to enhance cognitive
                      performance and long-term potentiation in wild-type animals
                      and in a mouse model for Alzheimer's disease. Systemic
                      administration of JQ1 elicited a hippocampal gene expression
                      program that is associated with ion channel activity,
                      transcription and DNA repair. Our findings suggest that JQ1
                      could be used as a therapy against dementia and should be
                      further tested in the context of learning and memory.},
      keywords     = {Alzheimer Disease: genetics / Amyloid beta-Protein
                      Precursor: genetics / Animals / Azepines: administration
                      $\&$ dosage / Behavior, Animal: drug effects / Chromosomal
                      Proteins, Non-Histone: antagonists $\&$ inhibitors / Gene
                      Expression: drug effects / Hippocampus: drug effects /
                      Hippocampus: metabolism / Hippocampus: physiology /
                      Long-Term Potentiation: drug effects / Male / Memory: drug
                      effects / Memory: physiology / Mice, Inbred C57BL / Mice,
                      Transgenic / Nuclear Proteins: antagonists $\&$ inhibitors /
                      Transcription Factors: antagonists $\&$ inhibitors /
                      Triazoles: administration $\&$ dosage / (+)-JQ1 compound
                      (NLM Chemicals) / Amyloid beta-Protein Precursor (NLM
                      Chemicals) / Azepines (NLM Chemicals) / BRDT protein, mouse
                      (NLM Chemicals) / Brd2 protein, mouse (NLM Chemicals) / Brd3
                      protein, mouse (NLM Chemicals) / Brd4 protein, mouse (NLM
                      Chemicals) / Chromosomal Proteins, Non-Histone (NLM
                      Chemicals) / Nuclear Proteins (NLM Chemicals) /
                      Transcription Factors (NLM Chemicals) / Triazoles (NLM
                      Chemicals)},
      cin          = {AG Fischer / AG Bonn 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1410002 / I:(DE-2719)1440012},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:28949335},
      pmc          = {pmc:PMC5639246},
      doi          = {10.1038/tp.2017.202},
      url          = {https://pub.dzne.de/record/139529},
}