Illi Ari, Kampman Olli, Hänninen Kari, Anttila Sami, Mattila Kari M, Katila Heikki, Rontu Riikka, Hurme Mikko, Lehtimäki Terho, Leinonen Esa
University of Tampere, Medical School, and Tampere University Hospital, Department of Psychiatry, Finland.
Hum Psychopharmacol. 2007 Jun;22(4):211-5. doi: 10.1002/hup.841.
Catechol-O-methyltransferase (COMT) gene has been investigated as a possible candidate gene in schizophrenia. The most studied polymorphism has been the functional val108/158met polymorphism of this COMT gene. There is also some evidence that this polymorphism could be related to drug response to antipsychotics in schizophrenia. COMT enzyme inactivates dopamine and noradrenaline. Based mainly on the original dopamine theory of schizophrenia, our primary hypothesis was that the maintenance dose of antipsychotics would be higher in patients with the low activity COMT genotype. In this study we evaluated the current daily dosage of antipsychotics in 180 patients with schizophrenia in connection with the COMT genotype. We could not demonstrate any clearly significant effect of this particular COMT genotype in relation to the daily maintenance dosages of antipsychotics in patients with schizophrenia.
儿茶酚-O-甲基转移酶(COMT)基因已被作为精神分裂症可能的候选基因进行研究。该COMT基因研究最多的多态性是功能性val108/158met多态性。也有一些证据表明这种多态性可能与精神分裂症患者对抗精神病药物的反应有关。COMT酶可使多巴胺和去甲肾上腺素失活。主要基于精神分裂症最初的多巴胺理论,我们的主要假设是,COMT基因低活性基因型患者的抗精神病药物维持剂量会更高。在本研究中,我们评估了180例精神分裂症患者当前的抗精神病药物每日剂量与COMT基因型的关系。我们未能证明这种特定的COMT基因型与精神分裂症患者抗精神病药物的每日维持剂量有任何明显的显著影响。