Ikeda Masashi, Ozaki Norio, Yamanouchi Yoshio, Suzuki Tatsuyo, Kitajima Tsuyoshi, Kinoshita Yoko, Inada Toshiya, Iwata Nakao
Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi 470-1192, Japan.
Schizophr Res. 2007 Mar;91(1-3):22-6. doi: 10.1016/j.schres.2006.12.020. Epub 2007 Feb 14.
Postmortem studies regarding schizophrenia revealed altered expression of genes related to gamma-amino butyric acid neurotransmission system. One of the most consistent findings is the reduced level of 67 kDa glutamic acid decarboxylase isoform (GAD(67)). Moreover, several studies reported positive associations between the GAD(67) gene (GAD1) and schizophrenia. These reasons, motivated us to carry out replication study regarding association between GAD1 (fourteen tagging SNPs) and schizophrenia in Japanese population (562 schizophrenic patients and 470 controls). However we couldn't confirm significant association that had been previously reported. Considering size of our sample and strategy that corresponds well with the approaches used in gene-based association analysis, our conclusion is that GAD1 does not play a major role in schizophrenia in Japanese population.
关于精神分裂症的尸检研究显示,与γ-氨基丁酸神经传递系统相关的基因表达发生了改变。最一致的发现之一是67 kDa谷氨酸脱羧酶同工型(GAD(67))水平降低。此外,多项研究报道了GAD(67)基因(GAD1)与精神分裂症之间存在正相关。基于这些原因,我们开展了一项关于GAD1(14个标签单核苷酸多态性)与日本人群精神分裂症关联的重复研究(562例精神分裂症患者和470例对照)。然而,我们未能证实先前报道的显著关联。考虑到我们样本的规模以及与基于基因的关联分析中所使用方法高度契合的策略,我们的结论是,在日本人群中,GAD1在精神分裂症中并不起主要作用。