Objective: We aimed to find out the molecular assessment of the risk of Parkinson’s disease (PD) in tobacco exposure through the SNP and gene expression (SNCA, LRRK2 and PRKN genes) studies.

Background: Tobacco uses are associated with a risk of PD (Li et al., 2015). And genetic and environmental factor are linked to PD (Wirdefeldt et al., 2011). PD includes oxidative stress (Zuo et al., 2013).

Method: This was conducted a total number of 200 chewing tobacco exposures and 200 controls. The study was approved by the Medical Review Committe; informed written consent form was obtained from them. A demographic data was collected regarding the duration of tobacco use, type of tobacco use, Tremor, Stiffness, Slowness and Impaired balance. Genomic DNA was extracted from lymphocytes using SNP gene mutation and gene polymorphic variant analysis using PCR-RFLP technique and sequencing. RNA was extracted by the TRIZOL method and analysis of gene expression (alpha-synuclein (SNCA), LRRK2 gene and parkin (PRKN), studies.

Results: Demographic results were indicated that high level of tobacco chewers having the risk of PD. Some symptoms were find the PD risk among the Tremor, Stiffness, Slowness and Impaired balance was documented in tobacco chewers. SNP analysis there is no novel mutation was found in the mild chewers and controls. Gene expression profiling of SNCA, LRRK2 gene and PRKN genes a significant alterations were identified in tobacco users with the PD risked samples.

Conclusion: In the present analysis mild associations were found in the tobacco chewer with PD. Poor oral health is associated with inflammation it can promote the risk of PD. it associated with poor oral health. Significance of gene-environment interactions was reported. The SNCA gene is located on the long arm of chromosome 4 (4q21.3-22). The first described point mutation of SNCA determining the manifestation of PD. Further, the study populations need to be taken to educate or create awareness about the effects of the tobacco usage. Furthermore, it may be exploiting in the development of new targeted finder analysis for PD.

References: Wirdefeldt K, Adami HO, er al., Epidemiology and etiology of Parkinson’s disease: a review of the evidence. Eur J Epidemiol. 2011;26(Suppl 1):S1–58. Zuo L, Motherwell MS. The impact of reactive oxygen species and genetic mitochondrial mutations in Parkinson’s disease. Gene. 2013;532:18–23. 12. Li X, Li W, er al., Association between cigarette smoking and Parkinson’s disease: A meta-analysis. Arch Gerontol Geriatr. 2015;61:510–516.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/snp-assessment-and-gene-expression-analysis-of-alpha-synuclein-snca-lrrk2-gene-and-parkin-prkn-gene-in-chewing-tobacco-exposures-and-find-out-the-risk-of-parkinsons-disease/