Norio Ozaki

Nagoya University, Nagoya, Aichi, Japan

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Publications (434)1531.35 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background The use of cholinesterase inhibitors is recommended for the treatment of dementia with Lewy bodies (DLB) in the guidelines of the DLB Consortium. However, no consensus regarding therapeutic approaches for DLB-related visual hallucinations has been reached. To the best of our knowledge, an appropriate dose of donepezil for the treatment of DLB at each stage has not been discussed.Methods Eight patients suffering from DLB with visual hallucinations were treated with donepezil. We summarize the effects of donepezil on these visual hallucinations chronologically in all cases and discuss its efficacy and characteristics.ResultsDonepezil contributed to the complete disappearance of visual hallucinations in all cases, and its effects were maintained for more than 6 months. However, relapses of visual hallucinations also occurred in all cases. Against these relapses, an increased dose of donepezil was very effective in resolving them again in almost all cases in this study.Conclusions Donepezil was highly effective against visual hallucinations in DLB patients, but there were some issues regarding pharmacotherapy for DLB.
    Psychogeriatrics 01/2015; · 1.26 Impact Factor
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    ABSTRACT: Background: Nuclear distribution E homolog 1 (NDE1), located within chromosome 16p13.11, plays an essential role in microtubule organization, mitosis, and neuronal migration and has been suggested by several studies of rare copy number variants to be a promising schizophrenia (SCZ) candidate gene. Recently, increasing attention has been paid to rare single-nucleotide variants (SNVs) discovered by deep sequencing of candidate genes, because such SNVs may have large effect sizes and their functional analysis may clarify etiopathology. Methods and Results: We conducted mutation screening of NDE1 coding exons using 433 SCZ and 145 pervasive developmental disorders samples in order to identify rare single nucleotide variants with a minor allele frequency ≤5%. We then performed genetic association analysis using a large number of unrelated individuals (3554 SCZ, 1041 bipolar disorder [BD], and 4746 controls). Among the discovered novel rare variants, we detected significant associations between SCZ and S214F (P = .039), and between BD and R234C (P = .032). Furthermore, functional assays showed that S214F affected axonal outgrowth and the interaction between NDE1 and YWHAE (14-3-3 epsilon; a neurodevelopmental regulator). Conclusions: This study strengthens the evidence for association between rare variants within NDE1 and SCZ, and may shed light into the molecular mechanisms underlying this severe psychiatric disorder.
    Schizophrenia bulletin. 10/2014;
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    ABSTRACT: Blonanserin differs from currently used serotonin 5-HT2A/dopamine-D2 receptor antagonists in that it exhibits higher affinity for dopamine-D2/3 receptors than for serotonin 5-HT2A receptors. We investigated the involvement of dopamine-D3 receptors in the effects of blonanserin on cognitive impairment in an animal model of schizophrenia. We also sought to elucidate the molecular mechanism underlying this involvement. Blonanserin, as well as olanzapine, significantly ameliorated phencyclidine (PCP)-induced impairment of visual-recognition memory, as demonstrated by the novel object recognition test (NORT) and increased extracellular dopamine levels in the medial prefrontal cortex (mPFC). With blonanserin, both of these effects were antagonized by DOI (a serotonin 5-HT2A receptor agonist) and 7-OH-DPAT (a dopamine-D3 receptor agonist), whereas the effects of olanzapine were antagonized by DOI but not by 7-OH-DPAT. The ameliorating effect was also antagonized by SCH23390 (a dopamine-D1 receptor antagonist) and H-89 (a protein kinase A (PKA) inhibitor). Blonanserin significantly remediated the decrease in phosphorylation levels of PKA at Thr(197) and of NR1 (an essential subunit of N-methyl-d-aspartate (NMDA) receptors) at Ser(897) by PKA in the mPFC after a NORT training session in the PCP-administered mice. There were no differences in the levels of NR1 phosphorylated at Ser(896) by PKC in any group. These results suggest that the ameliorating effect of blonanserin on PCP-induced cognitive impairment is associated with indirect functional stimulation of the dopamine-D1-PKA-NMDA receptor pathway following augmentation of dopaminergic neurotransmission due to inhibition of both dopamine-D3 and serotonin 5-HT2A receptors in the mPFC.Neuropsychopharmacology accepted article preview online, 14 August 2014; doi:10.1038/npp.2014.207.
    Neuropsychopharmacology: official publication of the American College of Neuropsychopharmacology 08/2014; · 8.68 Impact Factor
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    ABSTRACT: YWHAE is a possible susceptibility gene for schizophrenia that encodes 14-3-3epsilon, a Disrupted-in-Schizophrenia 1 (DISC1)-interacting molecule, but the effect of variation in its genotype on brain morphology remains largely unknown.
    PLoS ONE 08/2014; 9(8):e103571. · 3.53 Impact Factor
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    ABSTRACT: Increasing evidence has implicated the role of Disrupted-in-Schizophrenia-1 (DISC1), a potential susceptibility gene for schizophrenia, in early neurodevelopmental processes. However, the effect of its genotype variation on brain morphologic changes related to neurodevelopmental abnormalities in schizophrenia remains largely unknown. This magnetic resonance imaging study examined the association between DISC1 Ser704Cys polymorphism and a range of brain neurodevelopmental markers [cavum septi pellucidi (CSP), adhesio interthalamica (AI), olfactory sulcus depth, and sulcogyral pattern (Type I, II, III, and IV) in the orbitofrontal cortex (OFC)] in an all Japanese sample of 75 schizophrenia patients and 87 healthy controls. The Cys carriers had significantly larger CSP than the Ser homozygotes for both schizophrenia patients and healthy controls. The Cys carriers also exhibited a reduction in the Type I pattern of the right OFC in the healthy controls, but not in the schizophrenia patients. The DISC1 Ser704Cys polymorphism did not affect the AI and olfactory sulcus depth in either group. These results suggested a possible role of the DISC1 genotype in the early neurodevelopment of human brains, but failed to show its specific role in the neurodevelopmental pathology of schizophrenia.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 08/2014; · 3.55 Impact Factor
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    ABSTRACT: Functional neuroimaging techniques are widely used to elucidate changes in brain activity, and various questionnaires are used to investigate psychopathological features in patients with eating disorders (ED). It is well known that social skills and interpersonal difficulties are strongly associated with the psychopathology of patients with ED. However, few studies have examined the association between brain activity and social relationships in patients with ED, particularly in patients with extremely low body weight.
    BMC Psychiatry 06/2014; 14(1):173. · 2.23 Impact Factor
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    ABSTRACT: AimResults from this randomized, placebo-controlled study of aripiprazole augmentation to antidepressant therapy (ADT) in Japanese patients with major depressive disorder (MDD) [ADMIRE study] revealed that aripiprazole augmentation was superior to ADT alone and was well tolerated. In subgroup analyses, we investigated the influence of demographic- and disease-related factors on the observed responses. We also examined how individual symptom improvement was related to overall improvement in MDD.Methods Data from ADMIRE study were analyzed. Subgroup analyses were performed on the primary outcome measures, mean change in the Montgomery-Åsberg Depression Rating Scale (MADRS) total score from the end of selective serotonin reuptake inhibitor (SSRI)/serotonin norepinephrine reuptake inhibitor (SNRI) treatment to the end of the randomized treatment.ResultsChanges in the MADRS total scores were consistently greater with aripiprazole than placebo in each of the subgroups. Efficacy was not related to gender, age, number of adequate ADT trials in the current episode, MDD diagnosis, number of depressive episode, duration of the current episode, age of the first depressive episode, time since the first depressive episode, type of SSRI/SNRI, or severity at the end of SSRI/SNRI treatment phase.Compared to placebo, aripiprazole resulted in significant and rapid improvement on 7 of the 10 MADRS items, including sadness.Conclusion These post-hoc analyses indicated that aripiprazole was effective for a variety of Japanese patients with MDD who had exhibited inadequate responses to ADT. Additionally, we suggest that aripiprazole significantly and rapidly improved the core depressive symptoms.
    Psychiatry and Clinical Neurosciences 06/2014; · 2.04 Impact Factor
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    ABSTRACT: The ubiquitin ligase F-box protein 45 (FBXO45) is critical for synaptogenesis, neuronal migration, and synaptic transmission. FBXO45 is included in the 3q29 microdeletion region that confers a significant risk for schizophrenia, as shown by rare structural variant studies. Thus, FBXO45 is considered a prominent candidate for mediating schizophrenia pathogenesis. Here, we investigated rare, deleterious single nucleotide variants (SNVs) as well as small insertions and deletions (INDELs) in FBXO45 that may contribute to schizophrenia susceptibility. Using Sanger sequencing, we performed mutation screening in FBXO45 exon regions in 337 schizophrenia patients. Novel missense or nonsense variants were followed up with a genetic association study in an independent sample set of 601 schizophrenia patients and 916 controls, a case report for assessing the clinical consequence of the mutations, a pedigree study for measuring mutation inheritance in the proband's family, bioinformatics analyses for evaluating mutation effect on protein structure and function, and mRNA expression analysis for examining mutation transcriptional influence on FBXO45 expression. One heterozygous, novel, and rare missense mutation (R108C) was identified in a single schizophrenia patient and in his healthy mother. At age 20, this patient was diagnosed with paranoid schizophrenia and carried some clinical features of 3q29 deletion phenotypes, including premorbid IQ decline. With follow-up genotyping, this mutation was not found in either the schizophrenia group (0/601) or the healthy control group (0/916). Bioinformatics analyses predicted that R108C probably pathologically impacted the structure and function of the FBXO45 protein. The relative expression of FBXO45 in SCZ case with R108C mutation was relatively low when compared to 50 schizophrenia patients and 52 healthy controls. The R108C mutation in FBXO45 is a rare variant with a modest effect on schizophrenia risk that may disrupt the structure and function of the FBXO45 protein. Our findings also suggest that FBXO45 may be a new attractive candidate gene for schizophrenia.
    Schizophrenia Research 05/2014; · 4.59 Impact Factor
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    ABSTRACT: Recent genome-wide association studies (GWASs) of schizophrenia (SCZ) identified several susceptibility genes and suggested shared genetic components between SCZ and bipolar disorder (BD). We conducted a genetic association study of single nucleotide polymorphisms (SNPs) selected according to previous SCZ GWAS targeting psychotic disorders (SCZ and BD) in the Japanese population. Fifty-one SNPs were analyzed in a two-stage design using first-set screening samples (all SNPs: 1,032 SCZ, 1,012 BD, and 993 controls) and second-set replication samples (“significant” SNPs in the first-set screening analysis: 1,808 SCZ, 821 BD, and 2,321 controls). We assessed allelic associations between the selected SNPs and the three phenotypes (SCZ, BD, and “psychosis” [SCZ + BD]). Nine SNPs revealed nominal association signals for all comparisons (Puncorrected < 0.05), of which two SNPs located in the major histocompatibility complex region (rs7759855 in zinc finger and SCAN domain containing 31 [ZSCAN31] and rs1736913 in HLA-F antisense RNA1 [HLA-F-AS1]) were further assessed in the second-set replication samples. The associations were confirmed for rs7759855 (Pcorrected = 0.026 for psychosis; Pcorrected = 0.032 for SCZ), although the direction of effect was opposite to that in the original GWAS of the Chinese population. Finally, a meta-analysis was conducted using our two samples and using our data and data from Psychiatric GWAS Consortium (PGC), which have shown the same direction of effect. SNP in ZSCAN31 (rs7759855) had the strongest association with the phenotypes (best P = 6.8 × 10−5 for psychosis: present plus PGC results). These data support shared risk SNPs between SCZ and BD in the Japanese population and association between MHC and psychosis. © 2014 Wiley Periodicals, Inc.
    American Journal of Medical Genetics Part B Neuropsychiatric Genetics 05/2014; · 3.23 Impact Factor
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    ABSTRACT: Objective We attempted to investigate whether dehydroepiandrosterone sulfate (DHEA-S) levels are associated with remission of major depressive disorder by assessing scores on the 17-Item Structured Interview Guide for the Hamilton Depression before and after antidepressant treatment. Methods Plasma DHEA-S levels in 24 patients diagnosed with major depressive disorder on the basis of Diagnostic and Statistical Manual of Mental Disorders, fourth edition (text revision) before and after antidepressant treatment, and 24 healthy, gender-matched, and age-matched controls were measured using a radioimmunoassay kit. ResultsPlasma DHEA-S levels in patients were significantly higher than those in healthy controls. In patients who achieved remission after antidepressant treatment, plasma DHEA-S levels significantly declined compared with the levels before treatment. A significant correlation was observed between changes in DHEA-S levels and Absence of Depressive and Anxious Mood scores, which are calculated from the 2-Item Structured Interview Guide for the Hamilton Depression rating as follows: severity of depressive mood and anxiety in patients before and after antidepressant treatment. Conclusions These findings suggest that plasma DHEA-S levels can be used as a putative indicator of the state of remission in patients with major depressive disorder. Copyright © 2014 John Wiley & Sons, Ltd.
    Human Psychopharmacology Clinical and Experimental 03/2014; · 2.10 Impact Factor
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    ABSTRACT: An altered sulcogyral pattern in the orbitofrontal cortex (OFC) has been implicated in schizophrenia as a possible marker of abnormal neurodevelopment, while its genetic mechanism remains unknown. This magnetic resonance imaging study investigated the relationship between the polymorphism of YWHAE (rs28365859), a gene encoding 14-3-3epsilon that is a Disrupted-in-Schizophrenia 1 (DISC1)-interacting molecule associated with neuronal development, and the OFC subtypes of the 'H-shaped' sulcus (Types I, II, and III) in a Japanese sample of 72 schizophrenia patients and 86 healthy controls. The schizophrenia patients had significantly increased Type III (p=0.004) and decreased Type I (p=0.013) expression on the right hemisphere compared to the controls. The subjects carrying the protective C allele showed a decrease in Type III (p=0.005) and an increase in Type I (p=0.017) compared to the G allele homozygotes, especially for the healthy subjects in the left hemisphere. These results suggest a possible role for the YWHAE genotype in the early development of the OFC sulcogyral pattern, but its effect alone is not likely to explain the altered sulcogyral pattern in schizophrenia.
    Progress in Neuro-Psychopharmacology and Biological Psychiatry 02/2014; · 3.55 Impact Factor
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    ABSTRACT: Postnatal Depression has demonstrated long-term consequences on child cognitive and emotional development; however, the link between maternal and child pathology has not been clearly identified. We conducted a prospective study using self-rating questionnaires to clarify the association between bonding disorder and maternal mood during pregnancy and after childbirth. A total of 389 women participated in this study and completed questionnaires. Participants were asked to complete the Edinburgh Postnatal Depression Scale (EPDS) and the Mother-to-Infant Bonding Scale (MIB) four times during pregnancy and the postpartum period. We found statistically significant weak to moderate correlations (r=0.14-0.39) between the EPDS and MIB scores at each testing period. Women who experienced low mood tended to have stronger bonding disorder. Furthermore, the effectiveness of attachment between the mother and child was closely related to the mood of the mother as measured by the EPDS. We observed different patterns of bonding and maternal mood. Distinct subtypes regarding maternal mood and formation of mother-to-infant attachment suggests that analysis of bonding disorder should be performed considering the course of maternal depressive symptoms.
    Psychiatry and Clinical Neurosciences 02/2014; · 2.04 Impact Factor
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    ABSTRACT: Emotional distress is considered to be higher in patients with head and neck cancer than other types of cancer. The present study aimed to identify predictors of the postoperative levels of depression in patients with head and neck cancer who have undergone surgery. Postoperative levels of depression were assessed at 3, 6 and 12 months after surgery. The preoperative factors that were significant predictors of the postoperative level of depression at each time point were extracted using multiple regression analyses. The preoperative level of depression was a significant predictor of the postoperative level of depression at the 3rd, 6th and 12th postoperative months. At the sixth postoperative month, negative adjustment to cancer at baseline was also a significant predictor of the postoperative level of depression. Evaluating the level of depression and negative adjustment before surgery is considered to be effective for identifying patients who will develop depression after surgery.
    Japanese Journal of Clinical Oncology 02/2014; · 1.90 Impact Factor
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    ABSTRACT: The superior frontal gyrus (SFG), an area of the brain frequently found to have reduced gray matter in patients with schizophrenia, is involved in self-awareness and emotion, which are impaired in schizophrenia. However, no genome-wide association studies of SFG volume have investigated in patients with schizophrenia. To identify single-nucleotide polymorphisms (SNPs) associated with SFG volumes, we demonstrated a genome-wide association study (GWAS) of gray matter volumes in the right or left SFG of 158 patients with schizophrenia and 378 healthy subjects. We attempted to bioinformatically ascertain the potential effects of the top hit polymorphism on the expression levels of genes at the genome-wide region. We found associations between five variants on 1p36.12 and the right SFG volume at a widely used benchmark for genome-wide significance (P<5.0 × 10(-8)). The strongest association was observed at rs4654899, an intronic SNP in the eukaryotic translation initiation factor 4 gamma, 3 (EIF4G3) gene on 1p36.12 (P=7.5 × 10(-9)). No SNP with genome-wide significance was found in the volume of the left SFG (P>5.0 × 10(-8)); however, the rs4654899 polymorphism was identified as the locus with the second strongest association with the volume of the left SFG (P=1.5 × 10(-6)). In silico analyses revealed a proxy SNP of rs4654899 had effect on gene expression of two genes, HP1BP3 lying 3' to EIF4G3 (P=7.8 × 10(-6)) and CAPN14 at 2p (P=6.3 × 10(-6)), which are expressed in moderate-to-high levels throughout the adult human SFG. These results contribute to understand genetic architecture of a brain structure possibly linked to the pathophysiology of schizophrenia.
    Translational psychiatry. 01/2014; 4:e472.
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    Psychiatry and Clinical Neurosciences 01/2014; 68(1):83-4. · 2.04 Impact Factor
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    ABSTRACT: The ubiquitin ligase F-box protein 45 (FBXO45) is critical for synaptogenesis, neuronal migration, and synaptic transmission. FBXO45 is included in the 3q29 microdeletion region that confers a significant risk for schizophrenia, as shown by rare structural variant studies. Thus, FBXO45 is considered a prominent candidate for mediating schizophrenia pathogenesis. Here, we investigated rare, deleterious single nucleotide variants (SNVs) as well as small insertions and deletions (INDELs) in FBXO45 that may contribute to schizophrenia susceptibility. Using Sanger sequencing, we performed mutation screening in FBXO45 exon regions in 337 schizophrenia patients. Novel missense or nonsense variants were followed up with a genetic association study in an independent sample set of 601 schizophrenia patients and 916 controls, a case report for assessing the clinical consequence of the mutations, a pedigree study for measuring mutation inheritance in the proband's family, bioinformatics analyses for evaluating mutation effect on protein structure and function, and mRNA expression analysis for examining mutation transcriptional influence on FBXO45 expression. One heterozygous, novel, and rare missense mutation (R108C) was identified in a single schizophrenia patient and in his healthy mother. At age 20, this patient was diagnosed with paranoid schizophrenia and carried some clinical features of 3q29 deletion phenotypes, including premorbid IQ decline. With follow-up genotyping, this mutation was not found in either the schizophrenia group (0/601) or the healthy control group (0/916). Bioinformatics analyses predicted that R108C probably pathologically impacted the structure and function of the FBXO45 protein. The relative expression of FBXO45 in SCZ case with R108C mutation was relatively low when compared to 50 schizophrenia patients and 52 healthy controls. The R108C mutation in FBXO45 is a rare variant with a modest effect on schizophrenia risk that may disrupt the structure and function of the FBXO45 protein. Our findings also suggest that FBXO45 may be a new attractive candidate gene for schizophrenia.
    Schizophrenia Research 01/2014; · 4.59 Impact Factor
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    ABSTRACT: The present study evaluated the reliability and concurrent validity of the new Tanaka B Intelligence Scale, which is an intelligence test that can be administered on groups within a short period of time.
    PLoS ONE 01/2014; 9(6):e100262. · 3.53 Impact Factor
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    ABSTRACT: The PTPRA gene, which encodes the protein RPTP-α, is critical to neurodevelopment. Previous linkage studies, genome-wide association studies, controlled expression analyses and animal models support an association with both schizophrenia and autism spectrum disorders, both of which share a substantial portion of genetic risks.
    PLoS ONE 01/2014; 9(11):e112531. · 3.53 Impact Factor
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    ABSTRACT: The Edinburgh Postnatal Depression Scale (EPDS) is a widely used screening tool for postpartum depression (PPD). Although the reliability and validity of EPDS in Japanese has been confirmed and the prevalence of PPD is found to be about the same as Western countries, the factor structure of the Japanese version of EPDS has not been elucidated yet.
    PLoS ONE 01/2014; 9(8):e103941. · 3.53 Impact Factor
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    ABSTRACT: Autism spectrum disorder is a neurodevelopmental disorder present in 1% of the population, characterized by impairments in reciprocal social interaction, communication deficits and restricted patterns of behavior. Approximately 10% of the autism spectrum disorder population is thought to have large chromosomal rearrangements. Copy-number variations (CNV) alter the genome structure either by duplication or deletion of a chromosomal region. The association between CNV and autism susceptibility has become more apparent through the use of methods based on comparative genomic hybridization in screening CNV. The nature of the high CNV rate in the human genome is partly explained by non-allelic homologous recombination between flanking repeated sequences derived from multiple copies of transposons or mobile genetic elements. There are hotspots for CNV in the human genome, such as 16p11.2 and 22q11.2. Genes involved in CNV are supposed to have copy-number dose-dependent effects on the behavior of affected individuals. Animal models give insight into the possible interactions between core genetic loci and additional factors contributing to the phenotypes of each individual. If affected genes code for cellular signaling molecules, reducing the dosage in the intracellular signaling pathway may result in the malfunction of the nervous system. The genetic background of autism spectrum disorder is highly heterogenic and most common or rare CNV do not lead to autism spectrum disorders in the majority of cases, but may occasionally increase the risk of developing an autism spectrum disorder.
    Psychiatry and Clinical Neurosciences 12/2013; · 2.04 Impact Factor

Publication Stats

6k Citations
1,531.35 Total Impact Points

Institutions

  • 2005–2014
    • Nagoya University
      • • Division of Psychiatry
      • • Graduate School of Medicine
      • • Graduate School of Environmental Studies
      Nagoya, Aichi, Japan
  • 2013
    • Social Insurance Chukyo Hospital
      Nagoya, Aichi, Japan
    • Chubu University
      • Department of Biomedical Sciences
      Kasugai, Aichi-ken, Japan
    • International University of Health and Welfare
      Otahara, Tochigi, Japan
  • 2009–2013
    • Niigata University
      • Division of Psychiatry
      Niahi-niigata, Niigata, Japan
    • Kamiiida Daiichi General Hospital
      Nagoya, Aichi, Japan
    • Nagoya City University
      • Graduate School of Natural Sciences
      Nagoya, Aichi, Japan
    • The University of Tokyo
      • Graduate School of Education
      Tokyo, Tokyo-to, Japan
    • Cardiff University
      • Department of Psychological Medicine and Neurology
      Cardiff, WLS, United Kingdom
  • 2012
    • Nanzan University
      Nagoya, Aichi, Japan
    • Tokyo Metropolitan Institute of Gerontology
      Edo, Tōkyō, Japan
    • Aichi Gakuin University
      Nagoya, Aichi, Japan
  • 2009–2012
    • Japan Science and Technology Agency (JST)
      Edo, Tōkyō, Japan
  • 2004–2012
    • Osaka City University
      • • Department of Neurosurgery
      • • Department of Public Health
      Ōsaka, Ōsaka, Japan
    • Kurume University
      • Department of Neuropsychiatry
      Kurume, Fukuoka-ken, Japan
  • 1997–2012
    • Fujita Health University
      • Department of Psychiatry
      Nagoya, Aichi, Japan
  • 2011
    • Osaka University
      • Molecular Research Center for Children's Mental Development
      Suika, Ōsaka, Japan
    • Wakayama University
      • Faculty of Systems Engineering
      Wakayama-shi, Wakayama-ken, Japan
    • Icahn School of Medicine at Mount Sinai
      Manhattan, New York, United States
  • 2008–2011
    • Meijo University
      • Graduate School of Pharmacy
      Nagoya-shi, Aichi-ken, Japan
    • Numazu City Hospital
      Sizuoka, Shizuoka, Japan
    • NEC Corporation
      Edo, Tōkyō, Japan
    • Chiba University
      • Department of Psychiatry
      Chiba-shi, Chiba-ken, Japan
    • Hokkaido University
      • Department of Psychiatry
      Sapporo-shi, Hokkaido, Japan
  • 2007–2011
    • University of Tsukuba
      • Department of Immunology and Medical Genetics
      Tsukuba, Ibaraki-ken, Japan
    • National Institute of Advanced Industrial Science and Technology
      • Network Photonics Research Center
      Tsukuba, Ibaraki, Japan
    • Nagoya Second Red Cross Hospital
      Nagoya, Aichi, Japan
  • 2004–2011
    • Kyushu University
      • • Medical Institute of Bioregulation - MIB Hospital
      • • Faculty of Pharmaceutical Sciences
      Fukuoka-shi, Fukuoka-ken, Japan
  • 2008–2009
    • University of Toyama
      • Department of Neuropsychiatry
      Тояма, Toyama, Japan
  • 2006–2009
    • Hamamatsu University School of Medicine
      • Research Center for Child Mental Development
      Hamamatsu, Shizuoka-ken, Japan
    • Internet Initiative Japan
      Edo, Tōkyō, Japan
  • 2003–2009
    • Okayama University
      • Department of Neuropsychiatry
      Okayama, Okayama, Japan
  • 1995–2004
    • National Institute on Alcohol Abuse and Alcoholism
      Maryland, United States
  • 2000
    • Otsu Red Cross Hospital
      Ōtu, Shiga, Japan
  • 1994–1998
    • National Institute of Mental Health (NIMH)
      • Laboratory of Clinical Science
      Maryland, United States