ReviewFrontiers in aging neuroscience2022
The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease.
Review in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Exploring the potential of miR-9a-5p in circadian rhythm and cognitive recovery following brain injury in neonatal rats.Functional & integrative genomics · 2025Article
- LncRNAs Orchestrating Neuroinflammation: A Comprehensive Review.Cellular and molecular neurobiology · 2025Review
- Deciphering the role of tRNA-derived fragments in neurological and psychiatric disease pathogenesis.Frontiers in cellular neuroscience · 2025Review
- Evaluating the neuroprotective potential ofIn silico pharmacology · 2025Article
- Small RNAs in plasma extracellular vesicles define biomarkers of premanifest changes in Huntington's disease.Journal of extracellular vesicles · 2024Article
- Mechanism and Therapeutic Prospect of miRNAs in Neurodegenerative Diseases.Behavioural neurology · 2023Review
- Associations Between Epigenetic Age Acceleration and microRNA Expression Among U.S. Firefighters.Epigenetics insights · 2023Article
- Optimized miR-124 reporters uncover differences in miR-124 expression among neuronal populationsFrontiers in neuroscience · 2023Article
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Authors and funding
6 authors.
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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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