| Project/Area Number |
16K10189
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Yamaguchi University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松尾 幸治 埼玉医科大学, 医学部, 教授 (00292912)
内田 周作 山口大学, 医学部附属病院, 講師 (10403669)
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| Project Period (FY) |
2016-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | うつ病 / 糖鎖 / バイオマーカー / Glycosylation / Depression |
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| Outline of Final Research Achievements |
Glycosylation, the addition of a carbohydrate moiety to a protein during biosynthesis, is a common post-translational modification involved in several disease states. Specific protein-glycan structures have been reported to be useful as biomarkers for cancer and some neuropsychiatric disorders; however, the relationship between glycosylation of plasma proteins and major depressive disorder (MDD) has not been studied. This study aimed to determine whether the plasma protein-glycan structure would differ in MDD from typical values, using both a stress-based mouse model and samples from patients with MDD. The glycan structure profile of plasma proteins might represent candidate biomarkers for MDD.
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| Academic Significance and Societal Importance of the Research Achievements |
うつ病患者の血漿タンパク質の糖鎖について調べ、うつ病患者で変化する糖鎖変化を見つけることが出来た。また、うつ病モデルマウスの血漿タンパク質でも、ストレス負荷を受けたマウスで変化している糖鎖変化を同定できた。今後、さらに詳しく血漿の糖鎖を調べることで、うつ病の診断につながるような検査方法が見つかる可能性がある。また、うつ病モデルマウスの脳内タンパク質の糖鎖を調べることで、うつ病の病態を引き起こす原因となるような糖鎖変化が見つかるかもしれない。
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