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Neurodegenerative disease

Histone deacetylase 4 promotes cytoplasmic huntingtin aggregation in mouse models of Huntington disease

Nature Reviews Neurology volume 10, page 4 (2014)Cite this article

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In the brains of mice with Huntington disease (HD), the transcriptional repressor histone deacetylase 4 (HDAC4) colocalizes with mutant huntingtin to form cytoplasmic inclusions, according to research reported in PLoS Biology. Mielcarek et al. found that an HDAC4 knock-down in these animals delayed the formation of these inclusions without affecting global transcriptional regulation or nuclear huntingtin aggregation. The knock-down also restored neuronal and synaptic function, ameliorated neurological impairments, and increased survival times. The researchers conclude that HDAC4 could represent a new target for small-molecule therapeutics in HD.

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References

  1. Mielcarek, M. et al. HDAC4 reduction: a novel therapeutic strategy to target cytoplasmic huntingtin and ameliorate neurodegeneration. PLoS Biol. 11, e1001717 (2013)

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Histone deacetylase 4 promotes cytoplasmic huntingtin aggregation in mouse models of Huntington disease. Nat Rev Neurol 10, 4 (2014). https://doi.org/10.1038/nrneurol.2013.264

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