Copy Number Variation in Schizophrenia in the Japanese Population

Background Copy number variants (CNVs) have been shown to increase the risk to develop schizophrenia. The best supported findings are at 1q21.1, 15q11.2, 15q13.3, and 22q11.2 and deletions at the gene neurexin 1 ( NRXN1 ). Methods In this study, we used Affymetrix 5.0 arrays to investigate the role...

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Published in:Biological psychiatry (1969) 2010-02, Vol.67 (3), p.283-286
Main Authors: Ikeda, Masashi, Aleksic, Branko, Kirov, George, Kinoshita, Yoko, Yamanouchi, Yoshio, Kitajima, Tsuyoshi, Kawashima, Kunihiro, Okochi, Tomo, Kishi, Taro, Zaharieva, Irina, Owen, Michael J, O'Donovan, Michael C, Ozaki, Norio, Iwata, Nakao
Format: Article
Language:English
Subjects:
16p13.1
1q21.1
Adult
Adult and adolescent clinical studies
Asian Continental Ancestry Group - genetics
Biological and medical sciences
Case-Control Studies
Deletion
DNA Copy Number Variations - genetics
duplication
Female
Gene Expression Profiling
Genetic Predisposition to Disease
Genetic Variation
Genome-Wide Association Study
Genotype
Humans
Japan
Male
Medical sciences
Middle Aged
NRXN1
Oligonucleotide Array Sequence Analysis - methods
Psychiatry
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Schizophrenia
Schizophrenia - genetics
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Summary:Background Copy number variants (CNVs) have been shown to increase the risk to develop schizophrenia. The best supported findings are at 1q21.1, 15q11.2, 15q13.3, and 22q11.2 and deletions at the gene neurexin 1 ( NRXN1 ). Methods In this study, we used Affymetrix 5.0 arrays to investigate the role of rare CNVs in 575 patients with schizophrenia and 564 control subjects from Japan. Results There was a nonsignificant trend for excess of rare CNVs in schizophrenia ( p = .087); however, we did not confirm the previously implicated association for very large CNVs (>500 kilobase [kb]) in this population. We provide support for three previous findings in schizophrenia, as we identified one deletion in a case at 1q21.1, one deletion within NRXN1 , and four duplications in cases and one in a control subject at 16p13.1, a locus first implicated in autism and later in schizophrenia. Conclusions In this population, we support some of the previous findings in schizophrenia but could not find an increased burden of very large (>500 kb) CNVs, which was proposed recently. However, we provide support for the role of CNVs at 16p13.1, 1q21.1, and NRXN1.
ISSN:0006-3223
1873-2402
DOI:10.1016/j.biopsych.2009.08.034