ArticleFrontiers in molecular neuroscience2025
Inhibition of class IIa HDACs reduces mutant HTT aggregation by affecting RNA stability.
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: 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, Methods: Here, we tested a set of novel class IIa HDAC inhibitors for their efficiency in two different HD models: an HD cell line model and a Results: The selective class IIa HDAC inhibitor 1a led to a significant reduction of HTT aggregation and ameliorated the disease phenotype Discussion: Our data suggest a so far unknown mode of action of HDAC class IIa inhibitors by affecting
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