The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease

Soudeh Ghafouri-Fard; Tayyebeh Khoshbakht; Bashdar Mahmud Hussen; Mohammad Taheri; Kaveh Ebrahimzadeh; Rezvan Noroozi

doi:10.3389/fnagi.2022.987174

The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease

Front Aging Neurosci. 2022 Sep 15:14:987174. doi: 10.3389/fnagi.2022.987174. eCollection 2022.

Authors

Soudeh Ghafouri-Fard¹, Tayyebeh Khoshbakht², Bashdar Mahmud Hussen^{3

4}, Mohammad Taheri^{5

6}, Kaveh Ebrahimzadeh⁷, Rezvan Noroozi⁸

Affiliations

¹ Department of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
² Phytochemistry Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
³ Department of Pharmacognosy, College of Pharmacy, Hawler Medical University, Erbil, Iraq.
⁴ Center of Research and Strategic Studies, Lebanese French University, Erbil, Iraq.
⁵ Institute of Human Genetics, Jena University Hospital, Jena, Germany.
⁶ Urology and Nephrology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
⁷ Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
⁸ Malopolska Centre of Biotechnology, Jagiellonian University, Krakow, Poland.

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.

Keywords: DNA methylation; Huntington’s disease; epigenetic age; lncRNA; miRNA.

Publication types

Review