| Project/Area Number |
16K09793
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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 |
Endocrinology
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| Research Institution | Tohoku University |
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Principal Investigator |
Uchida Katsuya 東北大学, 情報科学研究科, 助教 (40344709)
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| Co-Investigator(Kenkyū-buntansha) |
井樋 慶一 東北大学, 情報科学研究科, 教授 (60232427)
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| Project Period (FY) |
2016-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 甲状腺ホルモン / パルブアルブミン / MeCP2 / 甲状腺機能低下症 / 発達障害 / CUX1 / サーカディアンリズム / 神経発達障害 / 脳神経疾患 / 生理活性 / 神経科学 |
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| Outline of Final Research Achievements |
TH insufficiency during perinatal period showed a decrease in the expression of parvalbumin (PV) in the neocortex and the hippocampus of the pups at PD 14. A significant decrease in methyl CpG-binding protein 2 (MeCP2)-positive neuronal nuclei was also observed in cortical layer 2/3 of the cerebral cortex but not the hippocampus. The brains were then stained with CUX1, a maker for cortical layer 2/3. In comparison with normal mice, CUX1 signals were decreased in the somatosensory cortex of the hypothyroid mice. Since CUX1 regulates the formation of neuronal spine and the branching of the dendrites, the morphological failure being observed in hypothyroidism may attribute to the disproportionate expression of the molecule. Further, the hypothyroid mouse showed abnormal behavior related circadian rhythm. However molecular mechanisms are mostly unclear. Further studies are required to elucidate the molecular mechanisms.
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| Academic Significance and Societal Importance of the Research Achievements |
甲状腺ホルモン欠乏による組織・生理学的な変化は、いくつかの点で、自閉症や統合失調症と類似性が極めて高い。甲状腺ホルモン欠乏によるクレチン症は、適切な時期の治療を怠ると、精神遅滞を引き起こすことになる。本研究成果より、我々は、精神疾患と、この甲状腺モデルの間には、共通の分子基盤が存在するとの仮説に至った。精神機能発現における分子メカニズムの解明は社会的要請が強く、これは本研究の継続した展開を強く後押しするものである。
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