Study of the pathomechanism of neuroaxonal distrophy using iPLA2beta-deficient mouse
| Project/Area Number |
22790314
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
KOEI Shinzawa 大阪大学, 医学系・研究科, 助教 (70403186)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 神経軸索ジストロフィー / スフェロイド / 疾患モデルマウス / ミトコンドリア / ホスホリパーゼA2 / 脳神経疾患 / ノックアウトマウス / phospholipase A2 / パーキンソン病 |
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| Research Abstract |
Using iPLA2 beta-deficient mouse for an animal model of human neuroaxonal dystrophy, the pathomechanism was studied by pathological, biochemical and genetical analysis. It was found that the mitochondrial degeneration is implicated in the pathogenesis of neuroaxonal dystrophy and its control can delay of disease development. Based on these results, we could propose new strategy for the establishment of human neuroaxonal dystrophy therapy.
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Report
(3 results)
Research Products
(9 results)
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[Journal Article] Analysis of two major intracellular phospholipases A(2)(PLA(2)) in mast cells reveals crucial contribution of cytosolic PLA(2)α, not Ca(2+)-independent PLA(2)β, to lipid mobilization in proximal mast cells and distal fibroblasts2011
Author(s)
Ueno N, Taketomi Y, Yamamoto K, Hirabayashi T, Kamei D, Kita Y, Shimizu T, Shinzawa K, Tsujimoto Y, Ikeda K, Taguchi R, Murakami M
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Journal Title
J Biol Chem
Volume: 286
Pages: 37249-63
Related Report
Peer Reviewed
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