2015 Fiscal Year Final Research Report
The role of inositol hexakisphosphate kinases for the onset mechanism of amyotrophic lateral sclerosis
| Project/Area Number |
25430014
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Neurophysiology / General neuroscience
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| Research Institution | Tokai University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Keywords | 筋萎縮性側索硬化症 / イノシトール6リン酸キナーゼ2 / 脊髄前角細胞 |
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| Outline of Final Research Achievements |
To address the role of IP6K2 in amyotrophic lateral sclerosis (ALS), we investigated the expression level of IP6K2, employing G93A mutant human superoxide dismutase-1 over-expressing transgenic mice (Tg mice) as ALS. The specimens of spinal cords were obtained from Tg mice and week age-matched wild-type mice. We investigated the expression levels of IP6K2 on the genes and proteins in Tg and wild-type mice. The gene expression level of IP6K2 in Tg mice at postnatal 17 weeks around the onset of ALS symptoms was lower compared to that of wild-type mice, while at postnatal 12 weeks before the symptoms of ALS it was signifivantly higher compared to wild-type mice. In the immunohistochemistry against IP6K2, it was stained in the cytoplasm in Tg mice during each week-old. These findings suggest that IP6K2 might be activated in Tg mice before the onset of ALS. IP6K2 might be a pre-symptomatic biomarker for ALS.
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| Free Research Field |
神経内科
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