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Updated: Sep 28, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Smoking and Parkinson's disease: explanatory hypothesis
Mohamed Farouk Allam1, Amparo Serrano del Castillo, Rafael Fernández-Crehuet Navajas
1Department of Preventive Medicine and Public Health, Faculty of Medicine, University of Córdoba, Avda. Menéndez Pidal, s/n 14004 Córdoba, Spain. fm2faahm@lucano.uco.es
Abstract:
A systematic review was conducted to estimate the pooled risk of smoking for Parkinson's disease in Chinese populations. The four identified case-control studies had odds ratios with 95% confidence intervals nearly or overlapping unity. Pooled odds ratio of these studies was 0.77 with 95% confidence interval 0.60 to 0.97. It was suggested that smoking induces debrisoquine 4-hydroxylase, which is responsible for the metabolism of antipsychotic drugs and the detoxification of certain environmental toxins known to cause dopaminergic neural damage. This could be the explanation of these contradictory results as cytochrome P-450 CYP2D6 debrisoquine hydroxylase gene polymorphism is known to be much lower in Chinese than in Caucasian people. This systematic review raises concerns about generalization of the conclusion previously settled by many cohort and case-control studies.
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