医学部
Profile Information
- Affiliation
- School of Medicine, Fujita Health University
- Degree
- 博士（医学）(名古屋大学)
- J-GLOBAL ID
- 200901048638344557
- researchmap Member ID
- 5000024641
- External link
Education:
1993 Ph.D. (Dr of Medical Science) Nagoya University The Graduate School of Medicine
(Prof. Toshiharu Nagatsu)
1989 M.D. Nagoya University School of Medicine
Professional training:
2017-present Vice president, Fujita Health University
2015-present Dean of the School of Medicine, Fujita Health University
2003-present Professor, Dep. Psychiatry, Fujita Health University School of Medicine
2002-2003 Assoc. Prof. Dep. Psychiatry, Fujita Health University School of Medicine
1998-2002 Assit. Prof. Dep. Psychiatry, Fujita Health University School of Medicine
(Prof. Norio Ozaki)
1996-1998 Visiting Fellow, Lab. Neurogenetics, NIAAA/NIH
(Dr. David Goldman)
1994-1996 Medical Staff, Dep. Psychiatry, Nagoya University School of Medicine
(Prof. Tatsuro Ohta)
1993-1994 Clinical Fellow in Medicine, North Hospital, Nagoya
1989-1990 Resident in Medicine, Kyoritsu General Hospital, Nagoya
Research field
Psychiatric genetics, Pharmacogenetics, Clinical psychopharmacology
NAKAO IWATA, M.D., Ph.D. is Professor of Psychiatry Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, JAPAN. He attended medical school and graduate school at Nagoya University and majored molecular neurochemistry and clinical psychiatry. He has published on many topics, including psychiatric genetics, pharmacogenomics, and clinical neuropsychopharmacology.
1993 Ph.D. (Dr of Medical Science) Nagoya University The Graduate School of Medicine
(Prof. Toshiharu Nagatsu)
1989 M.D. Nagoya University School of Medicine
Professional training:
2017-present Vice president, Fujita Health University
2015-present Dean of the School of Medicine, Fujita Health University
2003-present Professor, Dep. Psychiatry, Fujita Health University School of Medicine
2002-2003 Assoc. Prof. Dep. Psychiatry, Fujita Health University School of Medicine
1998-2002 Assit. Prof. Dep. Psychiatry, Fujita Health University School of Medicine
(Prof. Norio Ozaki)
1996-1998 Visiting Fellow, Lab. Neurogenetics, NIAAA/NIH
(Dr. David Goldman)
1994-1996 Medical Staff, Dep. Psychiatry, Nagoya University School of Medicine
(Prof. Tatsuro Ohta)
1993-1994 Clinical Fellow in Medicine, North Hospital, Nagoya
1989-1990 Resident in Medicine, Kyoritsu General Hospital, Nagoya
Research field
Psychiatric genetics, Pharmacogenetics, Clinical psychopharmacology
NAKAO IWATA, M.D., Ph.D. is Professor of Psychiatry Department of Psychiatry, Fujita Health University School of Medicine, Toyoake, Aichi, JAPAN. He attended medical school and graduate school at Nagoya University and majored molecular neurochemistry and clinical psychiatry. He has published on many topics, including psychiatric genetics, pharmacogenomics, and clinical neuropsychopharmacology.
Research Areas
1Research History
5Education
2-
1983 - 1989
Papers
642-
PCN reports : psychiatry and clinical neurosciences, 4(1) e70064, Mar, 2025BACKGROUND: With 30%-50% of people with bipolar depression (BDep) not responding to multiple pharmacological treatments, alternative therapies are needed. Accelerated intermittent theta burst stimulation (aiTBS) over the left dorsolateral prefrontal cortex (L-DLPFC) has been employed for individuals with pharmacological treatment-resistant major depressive disorder (TR-MDD). Imaging studies have revealed reduced regional activity of the L-DLPFC for both TR-MDD and pharmacological treatment-resistant BDep (TR-BDep), suggesting that aiTBS over the L-DLPFC may be beneficial for people with TR-BDep. METHODS: A 6-week, double-blind, sham-controlled, randomized trial will be conducted to compare the efficacy and safety of aiTBS to the L-DLPFC in people with TR-BDep (jRCTs042240019). Fifty iTBS sessions (1800 pulses/session) will be delivered in 10 daily sessions over 5 consecutive days at 90% resting motor threshold. This aiTBS protocol is termed as Fujita Neuromodulation Therapy for Bipolar Depression (FNT-BD). Twenty-two participants (both sexes, aged 18-64 years) with TR-BDep (DSM-5-TR, Type I) will be recruited. The response rate at any given week of follow-up will be the primary efficacy outcome, defined as a reduction of ≥50% in the Montgomery Åsberg Depression Rating Scale (MADRS) score. Other outcomes will include MADRS score changes, remission rate (10 ≥ MADRS score), Clinical Global Impression-Improvement score, Clinical Global Impression-Severity score, discontinuation rate, and incidence of individual adverse events. RESULTS: We anticipate that individuals who receive the aiTBS treatment show significant improvement in depressing symptoms compared to those receiving sham treatment. CONCLUSIONS: This study will provide valuable evidence for both patients with TR-BDep and clinicians.
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Translational psychiatry, 15(1) 63-63, Feb 20, 2025Suicidal ideation (SI) and behavior (SB) are major public health concerns, but risk factors for their development and progression are poorly understood. We used ICD codes and a natural language processing algorithm to identify individuals in a hospital biobank with SI-only, SB, and controls without either. We compared the profiles of SB and SI-only patients to controls, and each other, using phenome-wide association studies (PheWAS) and polygenic risk scores (PRS). PheWAS identified many risk factors for SB and SI-only, plus specific psychiatric disorders which may be involved in progression from SI-only to SB. PRS for suicide attempt were only associated with SB, and even after accounting for psychiatric disorder PRS. SI PRS were only associated with SI-only, although not after accounting for psychiatric disorder PRS. These findings advance understanding of distinct genetic and clinical risk factors for SB and SI-only, which will aid in early detection and intervention efforts.
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Pharmacopsychiatry, Jan 29, 2025The United States Food and Drug Administration approved the xanomeline-trospium combination in September 2024 for treating schizophrenia, based in part on three double-blind, randomized placebo-controlled trials in adults with schizophrenia experiencing acute psychosis. This random-effects model pairwise meta-analysis of those three trials found that xanomeline-trospium was comparable to placebo in terms of all-cause discontinuation, discontinuation rate due to adverse events, Simpson-Angus Scale score change, Barnes Akathisia Rating Scale score change, body weight change, body mass index change, blood pressure change, serum total cholesterol change, blood glucose change, QTc interval changes, and the incidence of headache, somnolence, insomnia, dizziness, akathisia, agitation, tachycardia, gastroesophageal reflux disease, diarrhea, increased weight, and decreased appetite. However, xanomeline-trospium was associated with a higher incidence of at least one adverse event, dry mouth, hypertension, nausea, vomiting, dyspepsia, and constipation, and increased serum triglyceride compared with placebo. Notably, xanomeline-trospium demonstrated superior efficacy than placebo in improving the Positive and Negative Syndrome Scale (PANSS) total score, PANSS positive subscale score, and PANSS negative subscale score.
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JMIR formative research, 9 e66330, Jan 29, 2025BACKGROUND: Estimating the prevalence of schizophrenia in the general population remains a challenge worldwide, as well as in Japan. Few studies have estimated schizophrenia prevalence in the Japanese population and have often relied on reports from hospitals and self-reported physician diagnoses or typical schizophrenia symptoms. These approaches are likely to underestimate the true prevalence owing to stigma, poor insight, or lack of access to health care among respondents. To address these issues, we previously developed an artificial neural network (ANN)-based schizophrenia classification model (SZ classifier) using data from a large-scale Japanese web-based survey to enhance the comprehensiveness of schizophrenia case identification in the general population. In addition, we also plan to introduce a population-based survey to collect general information and sample participants matching the population's demographic structure, thereby achieving a precise estimate of the prevalence of schizophrenia in Japan. OBJECTIVE: This study aimed to estimate the prevalence of schizophrenia by applying the SZ classifier to random samples from the Japanese population. METHODS: We randomly selected a sample of 750 participants where the age, sex, and regional distributions were similar to Japan's demographic structure from a large-scale Japanese web-based survey. Demographic data, health-related backgrounds, physical comorbidities, psychiatric comorbidities, and social comorbidities were collected and applied to the SZ classifier, as this information was also used for developing the SZ classifier. The crude prevalence of schizophrenia was calculated through the proportion of positive cases detected by the SZ classifier. The crude estimate was further refined by excluding false-positive cases and including false-negative cases to determine the actual prevalence of schizophrenia. RESULTS: Out of 750 participants, 62 were classified as schizophrenia cases by the SZ classifier, resulting in a crude prevalence of schizophrenia in the general population of Japan of 8.3% (95% CI 6.6%-10.1%). Among these 62 cases, 53 were presumed to be false positives, and 3 were presumed to be false negatives. After adjustment, the actual prevalence of schizophrenia in the general population was estimated to be 1.6% (95% CI 0.7%-2.5%). CONCLUSIONS: This estimated prevalence was slightly higher than that reported in previous studies, possibly due to a more comprehensive disease classification methodology or, conversely, model limitations. This study demonstrates the capability of an ANN-based model to improve the estimation of schizophrenia prevalence in the general population, offering a novel approach to public health analysis.
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Nature, Jan 22, 2025Bipolar disorder is a leading contributor to the global burden of disease1. Despite high heritability (60-80%), the majority of the underlying genetic determinants remain unknown2. We analysed data from participants of European, East Asian, African American and Latino ancestries (n = 158,036 cases with bipolar disorder, 2.8 million controls), combining clinical, community and self-reported samples. We identified 298 genome-wide significant loci in the multi-ancestry meta-analysis, a fourfold increase over previous findings3, and identified an ancestry-specific association in the East Asian cohort. Integrating results from fine-mapping and other variant-to-gene mapping approaches identified 36 credible genes in the aetiology of bipolar disorder. Genes prioritized through fine-mapping were enriched for ultra-rare damaging missense and protein-truncating variations in cases with bipolar disorder4, highlighting convergence of common and rare variant signals. We report differences in the genetic architecture of bipolar disorder depending on the source of patient ascertainment and on bipolar disorder subtype (type I or type II). Several analyses implicate specific cell types in the pathophysiology of bipolar disorder, including GABAergic interneurons and medium spiny neurons. Together, these analyses provide additional insights into the genetic architecture and biological underpinnings of bipolar disorder.
Misc.
634-
BIPOLAR DISORDERS, 24 58-59, Jul, 2022
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BIPOLAR DISORDERS, 23 48-48, Jun, 2021
Books and Other Publications
6
Research Projects
15-
Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science, Apr, 2022 - Mar, 2025
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Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science, Apr, 2016 - Mar, 2019
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Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science, Apr, 2013 - Mar, 2016
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Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science, 2010 - 2012
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Grants-in-Aid for Scientific Research, Japan Society for the Promotion of Science, 2008 - 2010