| Budget Amount *help |
¥18,070,000 (Direct Cost: ¥13,900,000、Indirect Cost: ¥4,170,000)
Fiscal Year 2013: ¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2012: ¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2011: ¥6,370,000 (Direct Cost: ¥4,900,000、Indirect Cost: ¥1,470,000)
Fiscal Year 2010: ¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
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| Research Abstract |
Our congenital ataxia mouse had genetic alterations in the vicinity of rs13476689 in chromosome 2. Mutation analysis identified 1653 mutations including SNP, insertion and deletion. In addition, 7048 bp deletion was found in the second intron of Gm13912 gene. These genetic alterations made it possible to genotype individual animals to maintain the strain. However, the responsible genetic alterations for ataxia could not be determined. Vacuolar degenerations found in the spinal and trigeminal nerves were the spheroid formation in the axon of NF200 positive neuron. The neurodegeneations had been occurred before the onset of the disease. Real-time PCR analysis of gene expression suggested that iron deposition in the kidney was caused by diminished divalent metal ion transporter.
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