| Budget Amount *help |
¥17,550,000 (Direct Cost: ¥13,500,000、Indirect Cost: ¥4,050,000)
Fiscal Year 2012: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2011: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2010: ¥7,150,000 (Direct Cost: ¥5,500,000、Indirect Cost: ¥1,650,000)
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| Research Abstract |
We previously demonstrated that Alzheimer's amyloid beta was an important causative factor for developing the age-related macular degeneration (AMD) by using neprilysin-deficient mice. Although this mouse developed the features of early AMD, such as the degeneration of retinal pigment epithelium (RPE) and drusen deposition, they did not develop the choroidal neovascularization, which was an important feature for late stage AMD. Thus, in the present study, we focused on the integrity of Bruch's membrane as well as a role of endothelial progenitor cells. As a key factor for disrupted integrity of Bruch's membrane, we examined the role of cathepsin L and HTRA-1 in the development of late stage AMD.
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