| Project/Area Number |
22659190
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
IKEDA Kazutaka 財団法人東京都医学総合研究所, 精神行動医学研究分野, 副参事研究員 (60281656)
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| Project Period (FY) |
2010 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,190,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | 自閉症 / 広汎性発達障害 / 結節性硬化症 / モデル動物 / 行動薬理学 / mTOR / ラパマイシン / トランスレーショナルリサーチ / 薬物療法 / シグナル伝達 |
|---|
| Research Abstract |
Drug therapy that effectively improves social interaction, a core symptom of autism, is awaited. Tuberous sclerosis complex(TSC) is caused by haploinsufficiency of the TSC1 or TSC2 gene, and is often manifested with autism. This study found in animal models of TSC, Tsc1^<+/-> and Tsc2^<+/-> mice, distinct autism-like behavioral features, and their recovery, as well as normalization of expression of multiple genes involved in mammalian target of rapamycin(mTOR) signaling, after treatment with an mTOR inhibitor, rapamycin. These findings indicate the crucial role of mTOR signaling in autism-like behaviors in mice, and suggests the usefulness of mTOR inhibitors in the pharmacological treatment of human autism.
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