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Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2018,9,11]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    In Huntington disease (HD) gene carriers the disease-causing mutant\n                    <jats:italic>Huntingtin<\/jats:italic>\n                    (m\n                    <jats:italic>HTT<\/jats:italic>\n                    ) is already present during early developmental stages, but, surprisingly, HD patients develop clinical symptoms only many years later. While a developmental role of\n                    <jats:italic>Huntingtin<\/jats:italic>\n                    has been described, so far new therapeutic approaches targeting those early neurodevelopmental processes are lacking. Here, we show that behavioral, cellular, and molecular changes associated with m\n                    <jats:italic>HTT<\/jats:italic>\n                    in the postnatal period of genetic animal models of HD can be reverted using low-dose treatment with a histone deacetylation inhibitor. Our findings support a neurodevelopmental basis for HD and provide proof of concept that pre-HD symptoms, including aberrant neuronal differentiation, are reversible by early therapeutic intervention in vivo.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1807962115","type":"journal-article","created":{"date-parts":[[2018,8,27]],"date-time":"2018-08-27T19:36:18Z","timestamp":1535398578000},"update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":61,"title":["Early postnatal behavioral, cellular, and molecular changes in models of Huntington disease are reversible by HDAC inhibition"],"prefix":"10.1073","volume":"115","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8411-8775","authenticated-orcid":false,"given":"Florian A.","family":"Siebzehnr\u00fcbl","sequence":"first","affiliation":[{"name":"McKnight Brain Institute, Department of Neurosurgery, University of Florida, Gainesville, FL 32611;"},{"name":"European Cancer Stem Cell 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