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Non-coding RNAs in Parkinson's disease: Regulating SNCA and alpha-synuclein aggregation.

Authors :
Thangavelu L
Moglad E
Afzal M
Almalki WH
Malathi H
Bansal P
Rani B
Walia C
Sivaprasad GV
Rajput P
Imran M
Source :
Pathology, research and practice [Pathol Res Pract] 2024 Sep; Vol. 261, pp. 155511. Date of Electronic Publication: 2024 Jul 30.
Publication Year :
2024

Abstract

Parkinson's disease is one of the vital neurodegenerative ailments attributed to a rise in Alpha-synuclein proteins leading to the advancement of motor and cognitive deterioration. Interestingly, in PD lncRNAs, miRNAs and siRNAs are also key regulators of SNCA and alpha-synuclein aggregation. This review will focus on the roles of these three types of small RNAs in trebling the development of PD through regulating SNCA expression or alpha-synuclein protein mediating the RNA from acting. Parkinson's disease is deļ¬ned by the build-up of alpha-synuclein protein resulting predominantly from the elevated expression level of the SNCA gene. Non-coding RNAs have gained broad appeal as fundamental modulators of gene expression and protein aggregation dynamics, with significant implications on the aetiology of PD. LncRNAs modulate SNCA transcription and edit epigenetic modifications, while miRNA target mRNA is involved in the stability and translation of count alpha-synuclein. Considering all these data, siRNAs can achieve the precise gene silencing effect that directly induces the downregulation of SNCA mRNA. This review also summarizes some recent reports about the interaction between these ncRNAs with the SNCA gene and alpha-synuclein protein, each through its independent in addition to synergistic mechanisms. This review highlights the possibility of therapeutic interventions to perturb SNCA expression to prevent alpha-synuclein aggregation via targeting ncRNAs that might be spun off novel drug development for PD.<br />Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Details

Language :
English
ISSN :
1618-0631
Volume :
261
Database :
MEDLINE
Journal :
Pathology, research and practice
Publication Type :
Academic Journal
Accession number :
39094523
Full Text :
https://doi.org/10.1016/j.prp.2024.155511