AI Article Synopsis

  • Huntington's disease (HD) is a genetic neurodegenerative disorder characterized by diverse symptoms, with recent research emphasizing the role of epigenetic changes in its onset and progression.
  • Studies indicate that non-coding RNAs, including a variety of microRNAs and long non-coding RNAs, play significant roles in how HD manifests and may be linked to the disease's pathology.
  • An increase in DNA methylation age has been identified as another important epigenetic marker associated with HD, highlighting the interplay of genetic and epigenetic factors in this condition.

Article Abstract

Huntington's disease (HD) is a dominantly inherited neurodegenerative disease with variable clinical manifestations. Recent studies highlighted the contribution of epigenetic alterations to HD progress and onset. The potential crosstalk between different epigenetic layers and players such as aberrant expression of non-coding RNAs and methylation alterations has been found to affect the pathogenesis of HD or mediate the effects of trinucleotide expansion in its pathophysiology. Also, microRNAs have been assessed for their roles in the modulation of HD manifestations, among them are miR-124, miR-128a, hsa-miR-323b-3p, miR-432, miR-146a, miR-19a, miR-27a, miR-101, miR-9*, miR-22, miR-132, and miR-214. Moreover, long non-coding RNAs such as DNM3OS, NEAT1, Meg3, and Abhd11os are suggested to be involved in the pathogenesis of HD. An accelerated DNA methylation age is another epigenetic signature reported recently for HD. The current literature search collected recent findings of dysregulation of miRNAs or lncRNAs as well as methylation changes and epigenetic age in HD.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9520620PMC
http://dx.doi.org/10.3389/fnagi.2022.987174DOI Listing

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