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No association of GSK3β gene ( GSK3B ) with Japanese schizophrenia
Author(s) -
Ikeda Masashi,
Iwata Nakao,
Suzuki Tatsuyo,
Kitajima Tsuyoshi,
Yamanouchi Yoshio,
Kinoshita Yoko,
Ozaki Norio
Publication year - 2005
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.30155
Subject(s) - single nucleotide polymorphism , gsk3b , linkage disequilibrium , gsk 3 , schizophrenia (object oriented programming) , genetic association , genetics , biology , gene , medicine , psychiatry , kinase , genotype
Several lines of evidence indicate that glycogen synthase kinase‐3β (GSK3β) is one of the candidates for schizophrenia‐susceptibility factor. However, it has not been reported the association analysis between GSK3β gene ( GSK3B ) and Japanese schizophrenia based on linkage disequilibrium (LD). We provide an association analysis using relatively large samples (381 schizophrenia, and 352 controls) after determination of “tag single nucleotide polymorphisms (SNPs).” In this LD mapping, we selected and genotyped for eight polymorphisms (seven SNPs and one diallelic (CAA) n repeat), which covered the entire region of GSK3B, and determined two “tag SNPs.” In the following association analysis using these two “tag SNPs,” we could not find association with Japanese schizophrenia. Furthermore, we also include subgroup analysis considering age‐at‐onset and subtypes, neither could we find associations. Because our samples provided quite high power, these results indicate that GSK3B may not play a major role in Japanese schizophrenia. © 2005 Wiley‐Liss, Inc.