Effect of Dopamine D2 Receptor Gene Polymorphism for Smoking in Patients with Schizophrenia.
- Author:
Hong Seock LEE
1
;
Seung Hyun KIM
;
Heon Jeong LEE
;
Tae Woo KIM
;
Duck Jung HAN
;
Yong Ku KIM
;
Leen KIM
;
Min Soo LEE
;
Bong Gi SON
Author Information
1. Department of Neuropsychiatry, Korea University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Heterosis;
Nicotine;
Schizophrenia;
Dopamine;
Gender-specific
- MeSH:
Alleles;
DNA;
Dopamine*;
Female;
Genotype;
Heterozygote;
Homozygote;
Humans;
Hybrid Vigor;
Male;
Nicotine;
Polymorphism, Restriction Fragment Length;
Prevalence;
Receptors, Dopamine D2*;
Schizophrenia*;
Smoke*;
Smoking*
- From:Journal of Korean Neuropsychiatric Association
2001;40(6):1231-1239
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: The authors examined the genetic effect of DRD2 Taq I polymorphism to the smoking in the Korean schizophrenics. Also this study examined molecular heterosis and gender difference in the genetic effect to smoking in schizophrenics. METHODS: The study subjects were composed of 167 schizophrenic patients, 96 smokers and 71 non-smokers. DRD2 Taq I RFLP genotyping was carried out with DNA extracted from subjects' blood samples. RESULTS: Among the total schizophrenics, the smokers were not significantly different from the non-smokers in respect to the frequency and prevalence of A1 allele, the genotype distribution, or frequency of heterozygotes. In male schizophrenics, genotype distribution of smoking patients differed significantly from non-smoking patients(p=0.010), with a higher prevalence of A1 allele (p=0.020) and frequency of heterozygotes(p=0.005). In male schizophrenics, A1A2 heterozygotes showed significantly higher smoking rate than A1A1 or A2A2 homozygotes and non-smokers were deficient in heterozygotes. The deviation from Hardy-Weinberg expectations was observed in male and female non-smokers with opposite directions. Moreover, highly significant differences were seen between male and female non-smokers in A1 prevalence(p=0.001), genotype distribution(p<0.00011), and frequency of heterozygotes(p<0.00003). CONCLUSION: No significant difference between smokers and non-smokers in the genotype distributions of the total sample could be explained by the gender difference in the genetic effect of DRD2 A1 allele to the smoking with opposite directions. Our findings support molecular heterosis at the DRD2 gene.
