| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
To investigate whether neuronal cell senescence contributes to the pathogenesis of age-associated neurodegenerative diseases, we analyzed the expression of cell senescence markers in cultured primary cortical neurons from E17 embryos of SAMP8 mice, a model for age-associated neurodegeneration. Primary neurons from mouse embryos were successfully maintained in serum-free media for up to 8 weeks. The ratio of senescence-associated β-galactosidase-positive neurons from SAMP8 mice was significantly increased after 28 days in vitro (DIV) when compared to those from control SAMR1 mice. The expression of γ-H2AX, a marker for DNA damage foci, was increased in nuclei of cultured neurons after 28 DIV, although no significant difference between neurons from SAMP8 and SAMR1 mice. Other cell senescence markers, such as heterochromatin-associated mH2A and lipid peroxidation product 4-HNE, did not show significant difference between neurons from SAMP8 and SAMR1 mice.
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