Debrisoquine hydroxylase and Parkinson's disease.
The relationship between the genotypes of Xba I and Bam H I restriction fragment length polymorphisms (RFLPs) at a gene for debrisoquine hydroxylase (CYP2D6) and phenotypes of the metabolic function of debrisoquine/sparteine, the EM and the PM in a healthy Japanese population was investigated. The genotypes of Xba I 11.5 kb and Xba I 44 kb-Bam H I 2.3 kb- were responsible for the Japanese PM. Genotype of Xba I RFLP at CYP2D6 locus was analyzed in 43 healthy individuals and 51 patients with IDP. The relative risk of IDP was 2.15 times more for individuals with the Xba I 44 kb allele compared to those without the allele (chi 2 = 4.149, d.f. = 1, p < 0.05) and it was 6.32 times greater for the Xba I 44 kb homozygotes than the Xba I 29 kb homozygotes (chi 2 = 4.935, d.f. = 1, p < 0.05). These data suggest that the PM for debrisoquine/sparteine hydroxylase might be one of the genetic factors making humans susceptible to IDP acquisition.[1]References
- Debrisoquine hydroxylase and Parkinson's disease. Kondo, I., Kanazawa, I. Advances in neurology. (1993) [Pubmed]
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