Analysis of genetic variations in the dopamine D1 receptor (DRD1) gene and antipsychotics-induced tardive dyskinesia in schizophrenia.
- Authors
- Lai, I-Ching; Mo, Geng-Han; Chen, Mao-Liang; Wang, Ying-Chieh; Chen, Jen-Yeu; Liao, Ding-Lieh; Bai, Ya-Mei; Lin, Chao-Cheng; Chen, Tzu-Ting; Liou, Ying-Jay
- Year
- 2011
- Journal
- European journal of clinical pharmacology
- PMID
- 21181138
- DOI
- 10.1007/s00228-010-0967-2
BACKGROUND: Dyskinesia is a kind of abnormal involuntary movement disorder that increases with age. The pathogenesis of dyskinesia may result from divergent changes in dopamine D1 receptors (DRD1) and dopamine D2 receptors (DRD2) in the brain while aging. Tardive dyskinesia (TD), a kind of dyskinesia, may develop after long-term antipsychotic treatment. Because the prevalence of TD also steadily increased with age, TD has been suggested to be the consequence of an imbalance between DRD1 and DRD2. We supposed that patients who develop TD may have genetic variants of DRD1 that cause the excitatory effects of DRD1 overwhelming the attenuated inhibitory effects of DRD2 after antipsychotic treatment. METHODS: In the present study, schizophrenic inpatients receiving long-term antipsychotic treatment were first assessed using the Abnormal Involuntary Movement Scale (AIMS), and only patients who were either free of any abnormal involuntary movements (non-TD group, AIMS =0) or who showed persistent TD (TD group) were enrolled. Finally, 382 patients were recruited (TD=220, non-TD=162) and three single nucleus polymorphisms (SNPs; rs5326, rs4532 and rs265975) of DRD1 were genotyped for each subject. RESULTS: Genotype frequency (%; AA/AG/GG) of rs4532 (TD: non-TD) was 61.4/35.8/2.8: 74.2/24.5/1.3. After genetic analyses, genotype GG showed significant association with TD (if OR=2.0, power (%)=98.5; if OR=1.5, power (%)=63.7; P=0.033). Haplotype frequency (%) CGC of rs5326-rs4532-rs265975 (TD: non-TD) was 19.0:13.7; and after haplotype-based analyses, haplotype CGC also showed significant association with TD (OR=1.4, permutation P=0.027). CONCLUSION: Our results indicate that the genotypic variants of DRD1 might play a role in the susceptibility of TD. Further replication in other countries or other populations is highly expected.
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| Dopaminergic Epistases in Schizophrenia. | Bosun A et al. | — | 2024 | → |
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| Candidate Genes Encoding Dopamine Receptors as Predictors of the Risk of Antipsychotic-Induced Parkinsonism and Tardive Dyskinesia in Schizophrenic Patients. | Vaiman EE et al. | — | 2021 | → |
| Genetic Factors Associated With Tardive Dyskinesia: From Pre-clinical Models to Clinical Studies. | Tsermpini EE et al. | — | 2021 | → |
| Genome wide study of tardive dyskinesia in schizophrenia. | Lim K et al. | — | 2021 | → |
| Expanding on possible mechanisms for tardive dyskinesia: A response to Ali, Roque, and Mallakh. | Lana Frankle BS | — | 2020 | → |
| Putative role of pharmacogenetics to elucidate the mechanism of tardive dyskinesia in schizophrenia. | Loonen AJ et al. | — | 2019 | → |
| Analysis of the Promoter Region of Human Dopamine Receptor D1. | Wu X et al. | — | 2018 | → |
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| Associations between a locus downstream DRD1 gene and cerebrospinal fluid dopamine metabolite concentrations in psychosis. | Andreou D et al. | — | 2016 | → |
| Pharmacogenetics of tardive dyskinesia: an updated review of the literature. | Lanning RK et al. | — | 2016 | → |
| DRD1 rare variants associated with tardive-like dystonia: a pilot pathway sequencing study in dystonia. | Groen JL et al. | — | 2014 | → |
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| Dopamine receptors and the pharmacogenetics of side-effects of stimulant treatment for attention-deficit/hyperactivity disorder. | Levy F et al. | — | 2013 | → |
| Genetic variation in the human brain dopamine system influences motor learning and its modulation by L-Dopa. | Pearson-Fuhrhop KM et al. | — | 2013 | → |
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| The aggregate effect of dopamine genes on dependence symptoms among cocaine users: cross-validation of a candidate system scoring approach. | Derringer J et al. | — | 2012 | → |