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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},
}