@article{Reisbitzer2025,
title = {Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability},
author = {Annika Reisbitzer and Cecilia Hollitzer and Adriana Geraci and Jessye Schaefer and Maximilian Burghaus and Jonas Bruns and Joachim Urban and Thomas Kurz and Sybille Krauß},
editor = {Frontiers in Molecular Neuroscience },
doi = {10.3389/fnmol.2025.1579194},
year = {2025},
date = {2025-06-18},
journal = {Frontiers in Molecular Neuroscience },
abstract = {Huntington’s disease (HD) is a fatal inherited neurological disorder for which there are no curative treatments available. Patients suffer from progressive impairment in cognitive and motor functions. Transcriptional dysregulation is a major molecular disease mechanism of HD. Transcription is regulated by a variety of epigenetic marks, including acetylation of histone proteins. This acetylation is controlled by opposing activities of histone acetyltransferases and histone deacetylases (HDACs). Based on recent observations that inhibition of HDACs can ameliorate disease phenotypes in different model systems ranging from cell culture to yeast, Drosophila and mouse models, the development of HDAC inhibitors as therapeutics for HD is promising. Recently, class IIa HDAC enzymes (4, 5, 7, 9) and specifically HDAC 4, have been identified as potential targets for the treatment of HD.},
keywords = {HDAC inhibitors, Huntington’s disease},
pubstate = {published},
tppubtype = {article}
}