Regulatory miR-SNP rs4636297A > G in miR-126 is linked to increased risk of rigidity feature in patients with Parkinson's disease.
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| Title: | Regulatory miR-SNP rs4636297A > G in miR-126 is linked to increased risk of rigidity feature in patients with Parkinson's disease. |
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| Authors: | Pooshani, Sheyda (AUTHOR), Azadmehr, Abbas (AUTHOR), Saadat, Payam (AUTHOR), Sepidarkish, Mahdi (AUTHOR), Daraei, Abdolreza (AUTHOR) |
| Source: | International Journal of Neuroscience. Dec2025, Vol. 135 Issue 12, p1436-1445. 10p. |
| Subjects: | Parkinson's disease, Single nucleotide polymorphisms, Symptoms, MicroRNA genetics, Biomarkers, MicroRNA, Joint stiffness, Genotypes |
| Abstract: | Introduction: A growing body of strong evidence shows that the dysfunction of miRNAs plays key roles in the development and progression of Parkinson's disease (PD), however, little data has been reported on the association of their SNPs with PD susceptibility. In this study, we investigated the association of regulatory miR-SNP rs4636297A > G with a functional effect on the expression of miRNA-126, as a key dysregulated miRNA in the PD, with the susceptibility and clinical features of the PD. Methods and materials: In current study, we included a population consisting of 120 patients with PD and 120 clinically healthy individuals, and their blood samples were taken. After extracting the DNAs, the genotyping of the miR-SNP rs4636297A > G was done through RFLP-PCR technique. Finally, the association of this SNP with the risk and clinical features of PD was determined. Results: Although the results showed that the two groups did not differ significantly in terms of allelic and genotype frequencies, it was clinically found that individuals with genotypes carrying the minor allele G (AG and GG genotypes) of the miR-SNP rs4636297A > G had an increased risk of developing rigidity feature in the PD compared to its homozygous major AA genotype (GG genotype; OR = 5.14, p = 0.038 & GA genotype; OR = 4.32, p = 0.032). Conclusion: We report for the first time a significant association of functional regulatory SNP rs4636297A > G in the miR-126 with the Parkinson's clinicopathology. Therefore, this miR-SNP can have a potential predictive biomarker capacity for rigidity in PD, although this hypothesis needs further investigation in the future. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Introduction: A growing body of strong evidence shows that the dysfunction of miRNAs plays key roles in the development and progression of Parkinson's disease (PD), however, little data has been reported on the association of their SNPs with PD susceptibility. In this study, we investigated the association of regulatory miR-SNP rs4636297A > G with a functional effect on the expression of miRNA-126, as a key dysregulated miRNA in the PD, with the susceptibility and clinical features of the PD. Methods and materials: In current study, we included a population consisting of 120 patients with PD and 120 clinically healthy individuals, and their blood samples were taken. After extracting the DNAs, the genotyping of the miR-SNP rs4636297A > G was done through RFLP-PCR technique. Finally, the association of this SNP with the risk and clinical features of PD was determined. Results: Although the results showed that the two groups did not differ significantly in terms of allelic and genotype frequencies, it was clinically found that individuals with genotypes carrying the minor allele G (AG and GG genotypes) of the miR-SNP rs4636297A > G had an increased risk of developing rigidity feature in the PD compared to its homozygous major AA genotype (GG genotype; OR = 5.14, p = 0.038 & GA genotype; OR = 4.32, p = 0.032). Conclusion: We report for the first time a significant association of functional regulatory SNP rs4636297A > G in the miR-126 with the Parkinson's clinicopathology. Therefore, this miR-SNP can have a potential predictive biomarker capacity for rigidity in PD, although this hypothesis needs further investigation in the future. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00207454 |
| DOI: | 10.1080/00207454.2024.2398571 |
