Gene-Gene and Gene-Environment Interaction on the Risk of Parkinson’s Disease
2014
Background: Even with numerous studies the cause of Parkinson’s disease (PD) remains elusive. It has been
hypothesized that interactions between genetic and environmental factors may play an important role in the pathogenesis
of PD.
Objectives: To examine the gene-gene and gene-environment interaction on PD risk with respect to gene polymorphism of
cytochrome P450 2D6 (CYP2D6) and glutathione S-transferases pi 1 (GSTP1), organochlorine pesticides (OCPs) and
metals.
Methods: This study included 70 patients of PD and 100 age-matched controls. The restriction fragment length polymorphism
was used for analysis of genetic polymorphism. OCPs and serum metal levels were estimated by using gas chromatography
and an autoanalyser respectively.
Results: The CYP2D6*4 mt and GSTP1 *B allelic variants were significantly associated with increase in PD risk. We
found a statistically significant difference in β -hexachlorocyclohexane (β-HCH), dieldrin, 1,1-dichloro-2,2-bis(pchlorophenyl)
ethylene (pp’-DDE) and copper levels between the patients and controls. We found significantly high levels
of β-HCH, dieldrin and pp’-DDE in the CYP2D6*4 mt allelic variants, β-HCH and pp’-DDE in the GSTP1*B allelic variants
and dieldrin in the GSTP1*C allelic variants when comparing CYP2D6*4 non-mt, GSTP1 non-*B and GSTP1 non-
*C allelic variants in patients of PD respectively.
Conclusion: This study demonstrates that the CYP2D6*4 and GSTP1 genes may be considered as candidate genes for PD
and they may also interact with β- HCH, dieldrin and pp’-DDE to influence the risk for PD.
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