Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population

Yasuhisa Fukuo, Taro Kishi, Tomo Okochi, Tsuyoshi Kitajima, Tomoko Tsunoka, Takenori Okumukura, Yoko Kinoshita, Kunihiro Kawashima, Yoshio Yamanouchi, Wakako Umene-Nakano, Hiroshi Naitoh, Toshiya Inada, Reiji Yoshimura, Jun Nakamura, Norio Ozaki, Nakao Iwata

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Abstract

Several investigations have reported that abnormalities in circadian rhythms might be related with the pathophysiology of psychiatric disorders, since many psychiatric patients have insomnia and sleep-awake disturbance. A recent animal study reported that Magel2, which encodes a member of the MAGE/necdin family of proteins, might be associated in the pathophysiology of psychiatric disorders. Magel2 gene knockout mice showed altered concentrations of both dopamine and serotonin in several parts of the brain compared with controls. In addition, the authors of that study detected a bilateral reduction in cortical volume in distinct regions of the Magel2 gene knockout mice brain, including focused regions in the parieto-temporal lobe of the cerebral cortex, the amygdala, the hippocampus, and the nucleus accumbens. These mice were also found to have hypoactivity and abnormalities in circadian rhythms. From this evidence, we considered Magel2 gene (MAGEL2) to be a good candidate gene for the pathophysiology of schizophrenia and mood disorder, and we conducted a case-control study among Japanese (731 schizophrenia patients, 465 MDD patients, 156 BP patients and 758 controls) using three tagging SNPs in MAGEL2 (rs850815, rs8920 and rs4480754), selected using the HapMap database. We did not find any association between MAGEL2 and schizophrenia, BP or MDD in allele/genotype-wise analysis or haplotype-wise analysis. Our results suggest that MAGEL2 may not play a role in the pathophysiology of schizophrenia and mood disorders in the Japanese population. A replication study using larger samples may be required for conclusive results, since our sample size was small and our study analyzed only three SNPs in MAGEL2.

Original languageEnglish
Pages (from-to)285-291
Number of pages7
JournalNeuroMolecular Medicine
Volume12
Issue number3
DOIs
Publication statusPublished - 01-09-2010

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Mood Disorders
Schizophrenia
Psychiatry
Gene Knockout Techniques
Circadian Rhythm
Knockout Mice
Population
Single Nucleotide Polymorphism
HapMap Project
Nucleus Accumbens
Brain
Sleep Initiation and Maintenance Disorders
Temporal Lobe
Amygdala
Cerebral Cortex
Sample Size
Haplotypes
Genes
Case-Control Studies
Hippocampus

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Neurology
  • Cellular and Molecular Neuroscience

Cite this

Fukuo, Yasuhisa ; Kishi, Taro ; Okochi, Tomo ; Kitajima, Tsuyoshi ; Tsunoka, Tomoko ; Okumukura, Takenori ; Kinoshita, Yoko ; Kawashima, Kunihiro ; Yamanouchi, Yoshio ; Umene-Nakano, Wakako ; Naitoh, Hiroshi ; Inada, Toshiya ; Yoshimura, Reiji ; Nakamura, Jun ; Ozaki, Norio ; Iwata, Nakao. / Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population. In: NeuroMolecular Medicine. 2010 ; Vol. 12, No. 3. pp. 285-291.
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abstract = "Several investigations have reported that abnormalities in circadian rhythms might be related with the pathophysiology of psychiatric disorders, since many psychiatric patients have insomnia and sleep-awake disturbance. A recent animal study reported that Magel2, which encodes a member of the MAGE/necdin family of proteins, might be associated in the pathophysiology of psychiatric disorders. Magel2 gene knockout mice showed altered concentrations of both dopamine and serotonin in several parts of the brain compared with controls. In addition, the authors of that study detected a bilateral reduction in cortical volume in distinct regions of the Magel2 gene knockout mice brain, including focused regions in the parieto-temporal lobe of the cerebral cortex, the amygdala, the hippocampus, and the nucleus accumbens. These mice were also found to have hypoactivity and abnormalities in circadian rhythms. From this evidence, we considered Magel2 gene (MAGEL2) to be a good candidate gene for the pathophysiology of schizophrenia and mood disorder, and we conducted a case-control study among Japanese (731 schizophrenia patients, 465 MDD patients, 156 BP patients and 758 controls) using three tagging SNPs in MAGEL2 (rs850815, rs8920 and rs4480754), selected using the HapMap database. We did not find any association between MAGEL2 and schizophrenia, BP or MDD in allele/genotype-wise analysis or haplotype-wise analysis. Our results suggest that MAGEL2 may not play a role in the pathophysiology of schizophrenia and mood disorders in the Japanese population. A replication study using larger samples may be required for conclusive results, since our sample size was small and our study analyzed only three SNPs in MAGEL2.",
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Fukuo, Y, Kishi, T, Okochi, T, Kitajima, T, Tsunoka, T, Okumukura, T, Kinoshita, Y, Kawashima, K, Yamanouchi, Y, Umene-Nakano, W, Naitoh, H, Inada, T, Yoshimura, R, Nakamura, J, Ozaki, N & Iwata, N 2010, 'Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population', NeuroMolecular Medicine, vol. 12, no. 3, pp. 285-291. https://doi.org/10.1007/s12017-010-8116-8

Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population. / Fukuo, Yasuhisa; Kishi, Taro; Okochi, Tomo; Kitajima, Tsuyoshi; Tsunoka, Tomoko; Okumukura, Takenori; Kinoshita, Yoko; Kawashima, Kunihiro; Yamanouchi, Yoshio; Umene-Nakano, Wakako; Naitoh, Hiroshi; Inada, Toshiya; Yoshimura, Reiji; Nakamura, Jun; Ozaki, Norio; Iwata, Nakao.

In: NeuroMolecular Medicine, Vol. 12, No. 3, 01.09.2010, p. 285-291.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population

AU - Fukuo, Yasuhisa

AU - Kishi, Taro

AU - Okochi, Tomo

AU - Kitajima, Tsuyoshi

AU - Tsunoka, Tomoko

AU - Okumukura, Takenori

AU - Kinoshita, Yoko

AU - Kawashima, Kunihiro

AU - Yamanouchi, Yoshio

AU - Umene-Nakano, Wakako

AU - Naitoh, Hiroshi

AU - Inada, Toshiya

AU - Yoshimura, Reiji

AU - Nakamura, Jun

AU - Ozaki, Norio

AU - Iwata, Nakao

PY - 2010/9/1

Y1 - 2010/9/1

N2 - Several investigations have reported that abnormalities in circadian rhythms might be related with the pathophysiology of psychiatric disorders, since many psychiatric patients have insomnia and sleep-awake disturbance. A recent animal study reported that Magel2, which encodes a member of the MAGE/necdin family of proteins, might be associated in the pathophysiology of psychiatric disorders. Magel2 gene knockout mice showed altered concentrations of both dopamine and serotonin in several parts of the brain compared with controls. In addition, the authors of that study detected a bilateral reduction in cortical volume in distinct regions of the Magel2 gene knockout mice brain, including focused regions in the parieto-temporal lobe of the cerebral cortex, the amygdala, the hippocampus, and the nucleus accumbens. These mice were also found to have hypoactivity and abnormalities in circadian rhythms. From this evidence, we considered Magel2 gene (MAGEL2) to be a good candidate gene for the pathophysiology of schizophrenia and mood disorder, and we conducted a case-control study among Japanese (731 schizophrenia patients, 465 MDD patients, 156 BP patients and 758 controls) using three tagging SNPs in MAGEL2 (rs850815, rs8920 and rs4480754), selected using the HapMap database. We did not find any association between MAGEL2 and schizophrenia, BP or MDD in allele/genotype-wise analysis or haplotype-wise analysis. Our results suggest that MAGEL2 may not play a role in the pathophysiology of schizophrenia and mood disorders in the Japanese population. A replication study using larger samples may be required for conclusive results, since our sample size was small and our study analyzed only three SNPs in MAGEL2.

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