title: Lack of association between MAGEL2 and schizophrenia and mood disorders in the Japanese population.
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.
authors.affiliation: Department of Pychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, Japan.
authors.forename: Yasuhisa
authors.initials: Y
authors.lastname: Fukuo
authors.forename: Taro
authors.initials: T
authors.lastname: Kishi
authors.forename: Tomo
authors.initials: T
authors.lastname: Okochi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Kitajima
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tsunoka
authors.forename: Takenori
authors.initials: T
authors.lastname: Okumukura
authors.forename: Yoko
authors.initials: Y
authors.lastname: Kinoshita
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Kawashima
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Yamanouchi
authors.forename: Wakako
authors.initials: W
authors.lastname: Umene-Nakano
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Naitoh
authors.forename: Toshiya
authors.initials: T
authors.lastname: Inada
authors.forename: Reiji
authors.initials: R
authors.lastname: Yoshimura
authors.forename: Jun
authors.initials: J
authors.lastname: Nakamura
authors.forename: Norio
authors.initials: N
authors.lastname: Ozaki
authors.forename: Nakao
authors.initials: N
authors.lastname: Iwata
mesh_terms: D000328:Adult; D000818:Animals; D044466:Asian People / Q000235:genetics / Q000523:psychology; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008297:Male; D051379:Mice; D008875:Middle Aged; D019964:Mood Disorders / Q000235:genetics* / Q000503:physiopathology; D020641:Polymorphism, Single Nucleotide; D011506:Proteins / Q000235:genetics*; D012559:Schizophrenia / Q000235:genetics* / Q000503:physiopathology; D055815:Young Adult; D047908:Intracellular Signaling Peptides and Proteins; D064267:Intrinsically Disordered Proteins
chemical_list: D011506:Proteins; C510822:MAGEL2 protein, human; D047908:Intracellular Signaling Peptides and Proteins; D064267:Intrinsically Disordered Proteins
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