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

α-突触核蛋白 帕金森病 小RNA 基因沉默 表观遗传学 基因表达 基因 基因表达调控 疾病 翻译(生物学) 小干扰RNA 生物 遗传学 信使核糖核酸 细胞生物学 计算生物学 核糖核酸 医学 病理
作者
Lakshmi Thangavelu,Ehssan Moglad,Muhammad Afzal,Waleed Hassan Almalki,H Malathi,Pooja Bansal,Bindu Rani,Chakshu Walia,G V Sivaprasad,Pranchal Rajput,Mohd Imran
出处
期刊:Pathology Research and Practice [Elsevier BV]
卷期号:261: 155511-155511 被引量:7
标识
DOI:10.1016/j.prp.2024.155511
摘要

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 defined 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.
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