| Project/Area Number |
22590129
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | Asahikawa Medical College |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Kazuo 旭川医科大学, 医学部, 教授 (20127533)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 臨床薬学 / パーキンソン病進行抑制薬 / オキシカム系 / NSAIDｓ / パーキンソン病 / 神経細胞死抑制 / オキシカム系NSAIDs / シグナル伝達 / 新規メカニズム / PI3kinase/Akt経路 / 新規治療薬 |
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| Research Abstract |
In this study, three oxicam-bearing non-steroidal anti-inflammatroy drugs(NSAIDs), such as meloxicam, piroxicam and tenoxicam, were identified to have novel neuroprotective mechanism of maintaining phosphatidylinositol 3-kinase(PI3K)/Akt signaling against MPP^+-induced toxicity using neuroblastoma SH-SY5Y cells. The other types of NSAIDs did not show neuroprotection in the same assays. In a chronic mouse model of Parkinson's disease, meloxicam ameliorated motor dysfunction and dopaminergic neurodegeneration by maintaining Akt-signaling. These results suggest that meloxicam would be a candidate agent as a disease-modifying drug for Parkinson's disease.
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