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Josephine Hoh, Ph.D.
Yale University
New Haven, CT
Title:
AMD Beyond Complement and Serine Protease Pathways
Non-Technical Title:
A study to examine genetic factors leading to AMD
Duration:
April 1, 2007 - March 31, 2010
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Summary: This study will characterize two new genetic risk factors related to wet and dry AMD
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Aparna Lakkaraju, Ph.D.
Weill Medical College of Cornell University
New York, NY
Title:
Apolipoprotein E And Cholesterol Lowering Drugs In Age-Related Macular Degeneration
Non-Technical Title:
Cholesterol homeostasis and age-related macular degeneration
Duration:
April 1, 2009 - March 31, 2011
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Summary: The specific aims outlined in this proposal will provide a cell biological understanding of the role of a protein called apolipoprotein E and the regulation of cholesterol levels in the retinal pigment epithelial (RPE) tissue of the eye). We will also investigate the potential of two promising drugs, statins and PPARgamma agonists, which are currently being used to treat, respectively, atherosclerosis and diabetes. These drugs will be tested for their ability to maintain cholesterol balance in the RPE.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Jinbo Liu, M.D.
Cleveland Clinic Foundation
Cleveland, OH
Title:
Identification of autoreactive T cells in AMD Patients
Non-Technical Title:
Immune mechanism underlying AMD
Duration:
April 1, 2008 - March 31, 2010
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Summary: The experiments in this proposal will address the mechanisms underlying immune attack in the retina. This information could lead to treatment approaches not currently available.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Md Nawajes Mandal, Ph.D.
University of Oklahoma Health Sciences Center
Oklahoma City, OK
Title:
Nutritional Supplement Of Phytochemical In Prevention Of AMD
Non-Technical Title:
Nutraceuticals In Prevention Of AMD
Duration:
April 1, 2009 - March 31, 2011
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Summary: The efficacy of known potent anti-inflammatory and anti-oxidative botanical compounds such as, curcumin, sulforaphane, and caffeic acid phenethyl ester (CAPE) will be tested in animal models of retinal degeneration. The protective effect of these compounds on cell death will also be tested in cultured retina-derived cells. The mechanism of action of these compounds in retinal protection will be determined. As age-related macular degeneration (AMD) develops from oxidative-stress and chronic inflammation, we hope to find a promising compound that can be tested further in pre-clinical and clinical trials.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Nancy Mangini, Ph.D.
The Trustees of Indiana University
Gary, IN
Title:
Role of melanin and a novel Na:Ca:K exchanger in AMD
Non-Technical Title:
Duration:
April 1, 2006 - June 30, 2010
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Summary:
More details
Program: Macular Degeneration
Award Type: Standard
$200,000
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Neal Peachey, Ph.D.
The Cleveland Clinic Foundation
Cleveland, OH
Title:
The Role of Complement Regulation in Maintaining Outer Retinal Integrity
Non-Technical Title:
Role of Complement Regulation in Age-Related Macular Degeneration
Duration:
April 1, 2008 - March 31, 2010
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Summary: The main goal of the study is to examine the phenotype of MCP1-/DAF- double knockout mice and to test whether light exposure exacerbates the phenotype.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Scott Plafker, Ph.D.
University of Oklahoma Health Sciences Center
Oklahoma City, OK
Title:
Countering Oxidative Stress In The Retina With The Ubiquitin System
Non-Technical Title:
Blocking Stress In Retinal Cells
Duration:
April 1, 2009 - March 31, 2011
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Summary: The aim of this application is to test the hypothesis that the ubiquitin system can be manipulated to augment the inherent anti-oxidant system present in retinal pigment epithelial (RPE) cells and photoreceptors. The ubiquitin system is one of the methods that cells use to destroy old or unnecessary proteins, and can be used to help regulate the activities of cellular protein. This hypothesis will be tested in mice using a virus to over-express a ubiquitin conjugating enzyme (UbcM2) coupled to a well-established, light-stress model of retinal degeneration.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Roxana Radu, M.D.
UCLA - Jules Stein Eye Institute
Los Angeles, CA
Title:
Analysis of A2E-degradation and Complement Activation in Two New Animals Models for Age-related Macular Degeneration
Non-Technical Title:
The Role of Lipofuscin Pigments and Chronic Inflammation as a Cause of Macular Degeneration
Duration:
April 1, 2008 - March 31, 2010
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Summary: This project will test the hypothesis that abnormal metabolism of vitamin A and its derivatives could lead to overt activation of the immune complement system. It will test this hypothesis using a well established animal model of macular defects. They will investigate the biochemical and molecular mechanisms used by the retina to deal with abnormal build-up of vitamin A-based toxic compounds.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Luba Robman, MBBS, Ph.D.
Centre for Eye Research Australia, The University of Melbourne
Melbourne, Australia
Title:
Genetic risks for AMD in Australians of Northern and Southern European origin
Non-Technical Title:
Genetic and environmental risks for age-related macular degeneration
Duration:
April 1, 2008 - March 31, 2010
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Summary: This study will investigate whether the risk of AMD, which is pre-determined by genes, can be modified by changes in diet. The study will genotype AMD cases and controls from a large Australian cohort of participants of Anglo-Celtic and Mediterranean origin to define genetic risk for AMD.
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Program: Macular Degeneration
Award Type: Standard
$100,000
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Steven Rosenzweig, Ph.D.
Medical University of South Carolina
Charleston, SC
Title:
IGF1R Crosstalk To VEGF Action In AMD And Cancer
Non-Technical Title:
Contributions Of Insulin-Like Growth Factor And Vascular Endothelial Growth Factor To Age-Related Macular Degeneration
Duration:
April 1, 2009 - March 31, 2010
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Summary: The goal of our studies is to demonstrate that Insulin-like Growth Factor (IGF-1) stimulated Vascular Endothelial Growth factor (VEGF) expression at the surface of the retinal pigment epithelial (RPE) leading to changes contributing to the delivery of VEGF to other areas of the eye. This, in turn, would be predicted to stimulate the growth of capillaries toward the RPE, and thus choroidal neovascularization (CNV), a hallmark of wet macular degeneration. Further, we will demonstrate that inhibition of IGF1, VEGFR-2 or FAK activation will reduce CNV in a mouse model.
More details
Program: Macular Degeneration
Award Type: Standard
$50,000
