| Project/Area Number |
15K15423
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Psychiatric science
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| Research Institution | Chiba University |
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Principal Investigator |
Kenji Hashimoto 千葉大学, 社会精神保健教育研究センター, 教授 (10189483)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIMA Tamaki 千葉大学, 社会精神保健教育研究センター, 特任助教 (00597130)
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| Research Collaborator |
FUJITA Yuko 千葉大学, 社会精神保健教育研究センター, 特任助教 (40623591)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脳・神経疾患 / 双極性障害 / バイオマーカー / クエン酸回路 / ミトコンドリア / 脳神経疾患 |
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| Outline of Final Research Achievements |
Although evidence for mitochondrial dysfunction in the pathogenesis of bipolar disorder (BD) has been reported, the precise biological basis remains unknown, hampering the search for novel biomarkers. In this study, we performed metabolomics of cerebrospinal fluid (CSF) from male BD patients and age-matched male healthy controls. After multivariate logistic regression, isocitric acid (isocitrate) was significantly higher in the CSF from BD patients than healthy controls. Furthermore, gene and protein expression of IDH3A in the postmortem brainfrom BD patients was higher than that of controls. These findings suggest that abnormality in the metabolism of isocitrate by IDH3A and IDH3B in the mitochondria plays a key role in the pathogenesis of BD, supporting the mitochondrial dysfunction hypothesis of BD. Therefore, IDH3 in the citric acid cycle may potentially be a novel therapeutic target for BD.
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