Genetics of tardive dyskinesia.

摘要: Tardive dyskinesia (TD) is one of the most serious adverse side effects antipsychotic drugs and an important topic pharmacogenetic studies. Since there a genetic susceptibility for developing this reaction, given that it hard to predict its development prior or during early period medication, study TD promising research has direct clinical application. Moreover, such studies would improve our understanding mechanism(s) underlying abnormal dyskinetic movement. A substantial number case-control association have been performed, with numbers focusing on genes involved in drug metabolism, as those cytochrome P450 (CYP) oxidative stress related well various neurotransmitter genes. These produced relatively consistent though controversial findings certain polymorphisms CYP2D6*10, DRD2 Taq1A, DRD3 Ser9Gly, HTR2A T102C, MnSOD Ala9Val. application genome-wide (GWAS) revealed associated previously were never considered be TD, rs7669317 4q24, GLI2 gene, GABA pathway genes, HSPG2 gene. Although investigated many positive not replicated are inconsistent, which could due differences design, sample size, and/or subject ethnicity. We expect more refined will performed future resolve these issues, then enable prediction thereof.