Copy Number Variation in Schizophrenia in the Japanese Population

Masashi Ikeda, Branko Aleksic, George Kirov, Yoko Kinoshita, Yoshio Yamanouchi, Tsuyoshi Kitajima, Kunihiro Kawashima, Tomo Okochi, Taro Kishi, Irina Zaharieva, Michael J. Owen, Michael C. O'Donovan, Norio Ozaki, Nakao Iwata

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Abstract

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.

Original languageEnglish
Pages (from-to)283-286
Number of pages4
JournalBiological Psychiatry
Volume67
Issue number3
DOIs
Publication statusPublished - 01-02-2010

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Schizophrenia
Population
Gene Deletion
Autistic Disorder
Japan

All Science Journal Classification (ASJC) codes

  • Biological Psychiatry

Cite this

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. / Copy Number Variation in Schizophrenia in the Japanese Population. In: Biological Psychiatry. 2010 ; Vol. 67, No. 3. pp. 283-286.
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abstract = "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.",
author = "Masashi Ikeda and Branko Aleksic and George Kirov and Yoko Kinoshita and Yoshio Yamanouchi and Tsuyoshi Kitajima and Kunihiro Kawashima and Tomo Okochi and Taro Kishi and Irina Zaharieva and Owen, {Michael J.} and O'Donovan, {Michael C.} and Norio Ozaki and Nakao Iwata",
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Ikeda, M, Aleksic, B, Kirov, G, Kinoshita, Y, Yamanouchi, Y, Kitajima, T, Kawashima, K, Okochi, T, Kishi, T, Zaharieva, I, Owen, MJ, O'Donovan, MC, Ozaki, N & Iwata, N 2010, 'Copy Number Variation in Schizophrenia in the Japanese Population', Biological Psychiatry, vol. 67, no. 3, pp. 283-286. https://doi.org/10.1016/j.biopsych.2009.08.034

Copy Number Variation in Schizophrenia in the Japanese Population. / 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.

In: Biological Psychiatry, Vol. 67, No. 3, 01.02.2010, p. 283-286.

Research output: Contribution to journalArticle

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T1 - Copy Number Variation in Schizophrenia in the Japanese Population

AU - Ikeda, Masashi

AU - Aleksic, Branko

AU - Kirov, George

AU - Kinoshita, Yoko

AU - Yamanouchi, Yoshio

AU - Kitajima, Tsuyoshi

AU - Kawashima, Kunihiro

AU - Okochi, Tomo

AU - Kishi, Taro

AU - Zaharieva, Irina

AU - Owen, Michael J.

AU - O'Donovan, Michael C.

AU - Ozaki, Norio

AU - Iwata, Nakao

PY - 2010/2/1

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N2 - 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.

AB - 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.

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