| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2016: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
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| Outline of Final Research Achievements |
To elucidate the mechanism for West syndrome, we investigated the pathogenesis of tuberous sclerosis complex (TSC), which is one of the causes of this syndrome. We have clarified a novel mechanism that Rheb activation, but not mTORC1, increases syntenin levels, which impairs dendritic spine morphology. Therefore, we reduced syntenin levels in TSC model mice, resulting in recovery of spine morphology and memory disorder. Next, to generate TSC model mice with spontaneous seizures, we deleted Tsc1 gene in the specific neurons or glial cells. We found some mice showed epilepsy and impaired memory. Finally, we found pharmacological inhibition of Rheb is effective for the symptoms of neuron- and glia-specific Tsc1 knockout mice.
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