| Budget Amount *help |
¥46,800,000 (Direct Cost: ¥36,000,000、Indirect Cost: ¥10,800,000)
Fiscal Year 2011: ¥8,840,000 (Direct Cost: ¥6,800,000、Indirect Cost: ¥2,040,000)
Fiscal Year 2010: ¥11,440,000 (Direct Cost: ¥8,800,000、Indirect Cost: ¥2,640,000)
Fiscal Year 2009: ¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
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| Research Abstract |
We performed basic research for three years(FY2009-2011) and achieved three key developments toward discovering drugs that that may be able to stop primary degenerative processes in spinocerebellar ataxia type 6(SCA6) and 31(SCA31). First, we found that the carboxyl-terminal fragment of the 1A-calcium channel is toxic when expressed in the cytoplasm. Second, we succeeded in developing a cellular model that could efficiently monitor the splicing patterns of the 1A-calcium channel gene. This model could be useful for future drug screens. Third, we found a penta-nucleotide sequence that is necessary for the development of SCA31. These achievements are crucial for the future establishment of treatments of SCA6 and SCA31.
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