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Teri Belecky-Adams, Ph.D.
Trustees of Indiana University
Indianapolis, IN
Title:
Bmp7 and glaucoma
Non-Technical Title:
The role of growth factor Bmp7 in gliosis and ganglion cell survival
Duration:
April 1, 2008 - March 31, 2010
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Summary: This study will focus on understanding the role of a growth factor, Bmp7, in both the increased survival of ganglion cells and the disruptive changes the glial cells undergo during glaucoma.
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Program: Glaucoma
Award Type: Standard
$100,000
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David Calkins, Ph.D.
Vanderbilt University Medical Center
Nashville, TN
Title:
TRPV1: A Novel Neuroprotective Target in Glaucoma
Non-Technical Title:
Targeting Neurobiological Sensitivity to Pressure in Glaucoma
Duration:
April 1, 2008 - March 31, 2010
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Summary: This research is aimed at understanding how optic nerve fibers respond to eye pressure and whether blunting this response could prevent vision loss in glaucoma. The study will also help identify new drugs to reduce optic nerve loss in glaucoma by making its fibers insensitive to eye pressure.
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Program: Glaucoma
Award Type: Standard
$100,000
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Mortimer Civan, M.D.
University of Pennsylvania
Philadelphia, PA
Title:
Pannexin regulation of aqueous humor inflow and outflow
Non-Technical Title:
Can pressure in the eye be reduced by altering release of ATP through newly-identified pannexin channels?
Duration:
April 1, 2008 - March 31, 2010
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Summary: The only approach proven to delay the onset and slow the progression of glaucoma is to lower eye pressure. The purine substances adenosine triphosphate (ATP) and adenosine (formed from ATP) are normally produced by cells in the eye, and participate in regulating eye pressure. The aim of this research is to identify how ATP is released at the two surfaces of the ciliary epithelium and also by cells of the aqueous humor outflow pathway, and to use this information to develop a new strategy for lowering eye pressure.
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Program: Glaucoma
Award Type: Standard
$100,000
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Jamie Craig, Ph.D.
Flinders University of South Australia
Adelaide, Australia
Title:
Genome Wide Association studies in Glaucoma using equimolar DNA pooling
Non-Technical Title:
Investigation of common genetic risk factors in glaucoma
Duration:
April 1, 2008 - March 31, 2010
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Summary: This research will identify common genetic markers that lead to glaucoma. The scientists will compare people with and without glaucoma to determine common gene variations and identify multiple genetic risk factors. They will prioritize genomic regions important in glaucoma. Understanding genetic factors for glaucoma could lead to earlier and better treatment for those at high risk and reduce the need for treatment for those at lower risk.
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Program: Glaucoma
Award Type: Standard
$100,000
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Adriana Di Polo, Ph.D.
University of Montreal
Montreal, Canada
Title:
Novel drug-based neuroprotective therapies for glaucoma
Non-Technical Title:
Novel neuroprotective strategies for glaucoma.
Duration:
April 1, 2008 - March 31, 2010
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Summary: This study will investigate the clinical potential of galantamine, a member of the acetylcholinesterase family, for the treatment of glaucoma. The study may lead to more effective drug-based therapies for treatment, and provide insight for the design of small molecule neuroprotective compounds with high specificity and few side effects.
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Program: Glaucoma
Award Type: Standard
$100,000
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C. Ethier, Ph.D.
Imperial College London
London, England
Title:
Suitability of Hydrostatic Pressure Model for Studying Glaucoma
Non-Technical Title:
Suitable Models for Glaucoma Research
Duration:
April 1, 2008 - March 31, 2010
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Summary: It has been previously shown that pressure has important effects on nerve cells in the eye. The way the pressure was applied to the cells in these previous studies may not be suitable for studying what occurs in glaucoma. This project will study whether this way of applying pressure to cells is useful for understanding the response of cells in glaucoma. They will repeat previous experiments, but will remove possible confounding effects. They will also measure oxygen levels and pH near the cells in a novel way that will help determine if the cells are being inadvertently exposed to a toxic environment in these experiments.
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Program: Glaucoma
Award Type: Standard
$100,000
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Nigar Fatma, Ph.D.
University of Nebraska Medical Center
Omaha, NE
Title:
Unveiling The Role Of Peroxiredoxin 6 In Maintaining Trabecular Meshwork Homeostasis
Non-Technical Title:
Treatment And Prevention Of Glaucoma By The Protein PRDX6
Duration:
April 1, 2009 - March 31, 2011
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Summary: Progression of glaucoma appears to be related to overstimulation of certain genes that control the matrix surrounding cells in a part of the eye, called the Trabecular Meshwork (TM).This overstimulation occurs when TM cells face oxidative stress due to reduced levels of antioxidant(s). By supplying Peroxiredoxin 6, PRDX6, an antioxidant protein, we will be able to restore these over modulated genes by blocking oxidative stress-induced deleterious signaling.
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Program: Glaucoma
Award Type: Standard
$93,991
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John Flanagan, Ph.D.
Toronto Western Hospital
Toronto, Canada
Title:
Protein expression of human optic nerve astrocytes and lamina cribrosa cells following exposure to different modes of biomechanical strain and hypoxia
Non-Technical Title:
Optic nerve cell reaction to different modes of strain and reduced oxygen
Duration:
April 1, 2008 - March 31, 2010
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Summary: This study will attempt to reproduce the stresses and strains that are likely present in the very earliest stages of glaucoma. The researchers will harvest cells from donated optic nerves and expose them to conditions similar to those found in early glaucoma. They will measure the responses by analyzing the different type of proteins the cells produce when stressed.
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Program: Glaucoma
Award Type: Standard
$100,000
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Brad Fortune, Ph.D.
Legacy Health System
Portland, OR
Title:
Imaging Retinal Nerve Fiber Layer Pathology in Experimental Glaucoma
Non-Technical Title:
Imaging Early Pathological Changes in Glaucoma
Duration:
April 1, 2008 - March 31, 2010
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Summary: This study will investigate whether degradation of subcellular components of the retinal nerve fiber layer can be clinically detectable and whether it precedes complete glaucoma related degeneration of neurons in the eye.
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Program: Glaucoma
Award Type: Standard
$100,000
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Haiyan Gong, M.D., Ph.D.
Boston University
Boston, MA
Title:
A Potential Target Site To Decrease Outflow Resistance
Non-Technical Title:
A Potential Target Site To Lower Eye Pressure In Glaucoma
Duration:
April 1, 2009 - March 31, 2011
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Summary: The goal of this study is to better understand the mechanisms involved in the regulation of aqueous outflow resistance in non-human and human eyes and to determine whether the connectivity between the inner wall of Schlemm's canal and underlying matrix in a portion of the eye, termed the trabecular meshwork, can be targeted to reduce outflow resistance, thus lowering intraocular pressure (IOP) in human eyes as it occurs in non-human eyes.
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Program: Glaucoma
Award Type: Standard
$100,000