Role of PON1 L55M Gene Polymorphism in Parkinson’s Disease among North Indian Population

Author:

Kumar Brijesh1,Saluja Alvee2,Juneja Abhishek3,Anand Kuljeet S3,Saraswathy Kallur N4,Longkumer Imnameren5,Dhamija Rajinder K2

Affiliation:

1. Department of Medicine, Lady Hardinge Medical College, New Delhi, India

2. Department of Neurology, Lady Hardinge Medical College and Smt. Suchita Kriplani Hospital, New Delhi, India

3. Department of Neurology, Dr RML Hospital, New Delhi, India

4. Department of Anthropology, University of Delhi, New Delhi, India

5. Laboratory of Biochemical and Molecular Anthropology, Department of Anthropology, University of Delhi, New Delhi, India

Abstract

Background and Objectives: The role of various genetic markers including alpha synuclein, Parkin, etc., is known in the pathogenesis of Parkinson’s disease (PD). Novel genetic markers including paraoxonase 1 (PON1) have also been linked to PD pathogenesis in recent studies. The PON1 L55M allele carriers may have defective clearance of environmental toxins and may result in increased susceptibility to PD. Hence, we studied the role of PON1 L55M polymorphism in PD among a North Indian population. Materials and Method: Seventy-four PD patients and 74 age- and sex-matched controls were recruited in this hospital-based case–control study. Baseline characteristics were recorded using structured questionnaire. DNA was extracted from 3–4 ml of venous blood, followed by PCR and restriction digestion. PON1 L55M genotypes were visualized as bands: LL (177 bp), LM (177, 140 bp) and MM (140,44 bp) on 3% agarose gel. Mann–Whitney U test and Chi-squared test were used for comparing two groups of skewed and categorical variables, respectively. Measures of strength of association were calculated by binary regression analysis. P value < 0.05 was considered as significant. Results: Parkinson’s disease patients had significantly higher exposure to pesticides (12.2%; P (organophosphate exposure) < 0.001) and well water drinking (28.4%; P = 0.006) compared to controls. Frequency distribution of LL, LM, MM genotypes was 67.5% (50/74), 28.4% (21/74), and 4.1% (3/74), respectively, for cases and 72.6% (54/74), 26% (19/74) and 1.4% (1/74), respectively, for controls. PON1 L55M genotype distribution between Parkinson’s disease cases and controls was not significant (P = 0.53). PON1 L55M polymorphism was not associated with PD after adjusting for confounders by binary regression analysis. Conclusion: There was no significant association between PON1 L55M polymorphism and PD. Larger population-based studies would be required from India before drawing any definite conclusions.

Publisher

Medknow

Reference25 articles.

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