Molecular mechanisms of the onset of schizophrenia-like phenotypes in chondroitin 6-sulfate-deficient mice
| Project/Area Number |
17K15096
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Functional biochemistry
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| Research Institution | Kobe Pharmaceutical University |
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Principal Investigator |
Naito Yuko 神戸薬科大学, 薬学部, 特任助教 (10456775)
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | コンドロイチン硫酸 / 糖鎖 / 統合失調症 / パルブアルブミン陽性細胞 / プロテオグリカン / 抑制性神経細胞 |
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| Outline of Final Research Achievements |
Glycans regulate various biological reactions. Not only a number of disease-specific changes in glycan structures have been reported, but also the failure to make these structures is linked to the onsets of various diseases. Our preliminary study revealed that knockout mice of one of the chondroitin sulfate (CS) sulfatase genes show schizophrenia-like phenotypes. To examine the underlying molecular mechanisms of these schizophrenia-like phenotypes caused by the altered sulfation of CS, detailed phenotypes of these mice were analyzed.
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| Academic Significance and Societal Importance of the Research Achievements |
統合失調症は、複数の遺伝的要因、環境要因が組み合わさって発症すると考えられており、発症の分子機構が未だ不明であることから、対症療法的治療が行われている。根本的な治療法確立のため、症状をもたらす分子メカニズムの解明が強く求められている。本研究により明らかにしたコンドロイチン硫酸の硫酸化異常がもたらす表現型を今後さらに詳しく解析することは、統合失調症の分子メカニズムの解明につながると期待される。
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Report
(3 results)
Research Products
(2 results)
