Association Study Between the Pericentrin (PCNT) Gene and Schizophrenia |
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Authors: | Shusuke Numata Masahito Nakataki Jun-ichi Iga Toshihito Tanahashi Yoshihiro Nakadoi Kazutaka Ohi Ryota Hashimoto Masatoshi Takeda Mitsuo Itakura Shu-ichi Ueno Tetsuro Ohmori |
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Institution: | 1. Department of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School, 3-8-15 Kuramoto-cho, Tokushima, 770-8503, Japan 2. Division of Genetic Information, Institute for Genome Research, The University of Tokushima Graduate School, Tokushima, Japan 3. Kagawa Prefectural Marugame Hospital, Kagawa, Japan 4. Department of Psychiatry, Osaka University Graduate School of Medicine, Osaka, Japan 5. The Osaka-Hamamatsu Joint Research Center for Child Mental Development, Osaka University Graduate School of Medicine, Osaka, Japan 6. Department of Neuropsychiatry, Ehime University School of Medicine, Ehime, Japan
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Abstract: | Disrupted-in-schizophrenia 1 (DISC1), a known genetic risk factor for schizophrenia (SZ) and major depressive disorder (MDD), interacts with several proteins and some of them are reported to be genetically associated with SZ. Pericentrin (PCNT) also interacts with DISC1 and recently single-nucleotide polymorphisms (SNPs) within the PCNT gene have been found to show significant associations with SZ and MDD. In this study, case-controlled association analysis was performed to determine if the PCNT gene is implicated in SZ. Nine SNPs were analyzed in 1,477 individuals (726 patients with SZ and 751 healthy controls). No significant difference was observed between the controls and the patients in allelic frequencies or genotypic distributions of eight SNPs. Although allelic distribution of rs11702684 was different between the two groups (P = 0.042), the difference did not reach statistical significance after permutation correction for multiple comparisons. In the haplotypic analysis, we could not find any significant association in our subjects, either. This gene may not play a major role independently in the etiology of SZ in the Japanese population. |
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