Association study between kynurenine 3-monooxygenase gene and schizophrenia in the Japanese population
Association study between kynurenine 3-monooxygenase gene and schizophrenia in the Japanese population
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DOI：
10.1111/j.1601-183x.2006.00231.x
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发表时间：
2006-06-01
影响因子：
2.5
通讯作者：
Ozaki, N.
中科院分区：
文献类型：
--
作者：
Aoyama, N.;Takahashi, N.;Ozaki, N.
几条证据表明犬尿烯酸（KYNA）途径的代谢变化与精神分裂症的病因有关。已知犬尿氨酸3-单加氧酶（KMO）的抑制剂会增加KYNA水平，KMO基因位于与精神分裂症相关的染色体区域1 q42-q44。单标记和单倍型分析6标签单核苷酸多态性（SNPs）的KMO进行（病例= 465，对照= 440）。通过单标记比较（P = 0.032）和包括该SNP的单倍型分析（P = 0.0049）观察到rs 2275163与精神分裂症的显著关联。使用第二组独立样本（病例= 480，对照= 448）（分别为P = 0.706和P = 0.689），未复制rs 2275163和单倍型的显著关联。这些结果表明，KMO不太可能与日本精神分裂症的发展有关。
Several lines of evidence suggest that metabolic changes in the kynurenic acid (KYNA) pathway are related to the etiology of schizophrenia. The inhibitor of kynurenine 3-monooxygenase (KMO) is known to increase KYNA levels, and the KMO gene is located in the chromosome region associated with schizophrenia, 1q42-q44. Single-marker and haplotype analyses for 6-tag single nucleotide polymorphisms (SNPs) of KMO were performed (cases = 465, controls = 440). Significant association of rs2275163 with schizophrenia was observed by single-marker comparisons (P = 0.032) and haplotype analysis including this SNP (P = 0.0049). Significant association of rs2275163 and haplotype was not replicated using a second, independent set of samples (cases = 480, controls = 448) (P = 0.706 and P = 0.689, respectively). These results suggest that the KMO is unlikely to be related to the development of schizophrenia in Japanese.