Establish model animal for AMD and Analysis of pathogenic mechanism of AMD
| Project/Area Number |
22791704
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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 |
Ophthalmology
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| Research Institution | 独立行政法人国立病院機構東京医療センター(臨床研究センター) (2011)
独立行政法人国立病院機構(東京医療センター臨床研究センター) (2010) |
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Principal Investigator |
AKAHORI Masakazu 独立行政法人国立病院機構東京医療センター(臨床研究センター), 分子細胞生物学研究部, 流動研究員 (30343544)
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 動物 / 細胞・組織 / 遺伝子 |
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| Research Abstract |
Age-related macular degeneration(AMD) is a common cause of blindness in the elderly. Genetic association in the 10q26(ARMS2/HTRA1) region has been established in many ethnic groups for dry-type AMD, typical wet-type AMD. Here, we describe the phenotypic characteristics of transgenic mice overexpressing HtrA1 or ARMS2.As a result, a vascularization was decreased in ARMS2mut transgenic mice. We show that a gene change of HtrA1 or ARMS2 have an effect of a vascularization.
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Report
(3 results)
Research Products
(10 results)
