Exploration of the regulatory mechanism of RNA binding protein for the dendritic spine pathology in schizophrenia
| Project/Area Number |
17K16394
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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 |
Psychiatric science
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| Research Institution | Nara Medical University |
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Principal Investigator |
KIMOTO Sohei 奈良県立医科大学, 医学部, 学内講師 (00405391)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2018: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 統合失調症 / RNA結合タンパク質 / staufen2 / 脳神経スパイン / アクチン細胞骨格 / 認知機能障害 / 前頭前野 / 棘突起（スパイン） / 細胞骨格 / 死後脳研究 / トランスレーショナルリサーチ |
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| Outline of Final Research Achievements |
Cognitive dysfunction is commonly observed in patiens with schizophrenia. In the prefrontal cortex (PFC) which is a core region in performing cognitive function, lower dendritic spine density and alterations of transcript expression such as actin-regulating genes and RGS4 have been reported to be observed in excitatory pyramidal neurons of PFC in schizophrenia.
Here, using postmortem brains, we examined whether RNA binding protein staufen2 (STAU2) that may regulate both actin-regulating genes and RGS4 can play a critical role in the molecular basis underlying cognitive deficit in schizophrenia. As a result, STAU2 expression in total gray matter of PFC did not differ between schizophrenia and controls. In conclusion, STAU2 expression may be altered in cortical layer- or cell-type specific manner. Alternatively, other molecular factors might contribute to the PFC dendritic spine pathology in schizophrenia.
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| Academic Significance and Societal Importance of the Research Achievements |
統合失調症では、難治性の認知機能障害が、患者の自立や社会復帰を妨げる大きな要因となっており、病態メカニズムの解明とそれに基づく効果的な治療法の開発が急務となっている。統合失調症患者で観察される前頭前野の錐体ニューロンの棘突起の変化に焦点を当て、当該疾患患者から得られた死後脳組織を用いて棘突起の形態や維持にとって鍵となる遺伝子を同定することを目的とし研究を行った。今後、本研究の成果を棘突起の機能回復を目指した認知機能障害の治療法の開発に役立てる。
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Report
(3 results)
Research Products
(5 results)
