Inhibition of KDM1A activity restores adult neurogenesis and improves hippocampal memory in a mouse model of Kabuki syndrome
Li Zhang, Genay Pilarowski, Emilio Merlo Pich, Atsushi Nakatani, John Dunlop, Rina Baba, Satoru Matsuda, Masaki Daini, Yasushi Hattori, Shigemitsu Matsumoto, Mitsuhiro Ito, Haruhide Kimura, Hans T. Björnsson
Abstract
mice demonstrated normalization of hippocampal memory defects. In summary, our data suggest that KDM1A inhibition is a plausible treatment strategy for KS and support the hypothesis that the epigenetic dysregulation secondary to KMT2D dysfunction plays a major role in the postnatal neurological disease phenotype in KS.
Topics & Concepts
DemethylaseDoublecortinNeurogenesisBiologyPhenocopyEpigeneticsHistone H3Cancer researchHistoneMethyltransferaseChromatin immunoprecipitationHippocampal formationHistone methylationHistone methyltransferaseKabuki syndromePhenotypeCell biologyDentate gyrusDNA methylationGeneticsNeuroscienceMethylationGene expressionGenePromoterEpigenetics and DNA MethylationGenetic Syndromes and ImprintingGenomics and Rare Diseases