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2014 Research Grants

Glaucoma Research Foundation provides seed money for creative pilot research projects that hold promise.

The National Institutes of Health and large companies may pass over the young researcher with an innovative idea, if there is no precedent. Armed with evidence made possible by our research grants, scientists can often secure the major funding necessary to bring their ideas to fruition.

We consider it vital to invest funds in new high-impact research that may lead to major government and philanthropic support. All Glaucoma Research Foundation grants to explore new ideas are in the amount of $40,000.

Following is a summary of projects we are currently funding.

The 2014 Shaffer Grants for Innovative Glaucoma Research

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Jeff M. Gidday, PhD
Washington University School of Medicine, St. Louis, Missouri

The Dr. Miriam Yelsky Memorial Research Grant

Project: Delayed Post-Conditioning for Glaucoma Neuroprotection

Summary: Protection of retinal neurons that die in glaucoma is a fundamental therapeutic strategy, but one that remains elusive. Although basic research documents that these cells die by a multi-factorial process, the vast majority of therapies tested to date, or in development, are likely to fail because they target only a single injury pathway. A novel way of approaching protection-based therapeutics for glaucoma should derive from evidence accumulating over two decades in stroke and cardiac arrest: That simultaneously activating a variety of self-defense responses in cells with stressful "conditioning" stimuli induces the expression of a host of genes that promote cell survival. We plan to test two such "epigenetics"-based therapeutic strategies in a model of glaucoma. If successful, our studies will provide a viable therapeutic strategy for saving vision in patients with glaucoma.

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Vikas Gulati, MD
Truhlsen Eye Institute, University of Nebraska Medical Center, Omaha, Nebraska

Project: Effect of Vascular Endothelial Growth Factor Blockers on Aqueous Humor Dynamics

Funding provided by a grant from The Alcon Foundation

Summary: Use of eye injections of drugs aimed at slowing the growth of abnormal blood vessels in the eye is becoming more common for the treatment of individuals with many eye problems including macular degeneration, diabetic retinopathy and retinal artery or vein blockage. Unfortunately, injections of these drugs can cause high eye pressure that may lead to glaucoma in some patients or make the control of high eye pressure more difficult in others. Considering the large number of people over the age of 40 who have glaucoma, many may be at particular risk of permanent vision loss from loss of pressure control when treated with these injections. Eye pressure by itself is determined by a delicate balance of fluid inflow and outflow from inside the eye. The effect of the injected drugs on any of these parameters has never been formally evaluated. The purpose of this study is to determine the effects of these drugs on the inflow and outflow of fluid from the eye and its consequences on eye pressure. Knowledge of the actual physiological effect of these drugs can have many benefits for glaucoma patients. For one it will help the eye doctor choose the optimal therapy to prevent the eye pressure elevation or to treat the high eye pressure if it does occur. Further research also will help determine which if any of these drugs is safer for glaucoma patients who also have abnormal blood vessel growth.

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David Krizaj, PhD
Moran Eye Institute, University of Utah, Salt lake City, Utah

Project: RGC Mechanotransduction as a Target in Glaucoma

Funding provided by Dr. James and Elizabeth Wise

Summary: The major diagnostic criterion for glaucoma is elevated pressure in the eye which identifies a proportion of patients that will develop this blinding disease. However, pressure-reducing drugs often help patients with elevated and normal intraocular pressure (IOP). The mechanism that is responsible for transducing the effects of eye pressure into degeneration of retinal ganglion cells (RGCs) is not known. Our proposal addresses this problem. We found that RGCs are the sole retinal neuron that express TRPV4, a pressure-sensitive channels that is permeable to calcium ions. This is intriguing because calcium is known to induce remodeling of cells and RGC degeneration in glaucoma. We will use molecular, histological, calcium imaging and electrophysiological methods to characterize the sensitivity of these channels to membrane stretch by mimicking the effect of IOP on RGC perikarya and axons. Second, we will characterize the effect of stretch on cells isolated from mouse glaucoma models. Third, we will study the effect of small molecule antagonist drugs to prevent stretch-mediated RGC degeneration and death. The study is strongly supported by preliminary evidence obtained in vitro and in vivo. Thus, the proposed work directly tackles the mechanosensitive disease mechanism in the posterior eye but also aims at developing new neuroprotective strategies.

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Yutao Liu, MD, PhD
Medical College of Georgia, Georgia Regents University, Augusta, Georgia

Project: Exosomal RNAs and Aqueous Humor Dynamics

Funding provided by a grant from The Alcon Foundation

Summary: The purpose of this study is to investigate the role of exosomes, small cell-manufactured vesicles secreted into bodily fluids including blood and the fluid in the eye called aqueous humor. Exosomes contain RNA, which is used to regulate cell function. Secreted RNAs have already been shown to be involved in cell-cell communication between different tissues/organs and to serve as biomarkers for human disorders, such as cancer. We will examine the characteristics of the RNA contained in exosomes in the aqueous humor with special emphasis on its function in exfoliation glaucoma, including the most common form of secondary open-angle glaucoma. This study may provide a potential biomarker and therapeutic targets for glaucoma.

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Stuart J. McKinnon, MD, PhD
Duke University Medical Center, Durham, North Carolina

Funding provided by Dr. James and Elizabeth Wise

Project: Neuroinflammation: The Role of Lymphocytes in Glaucoma

Summary: In glaucoma, permanent vision loss and blindness occur when retinal ganglion cells (RGCs) that make up the optic nerve are lost. Increasing evidence points to a central role of the immune system in the death of RGCs in glaucoma. A recent finding in our laboratory led to the novel hypothesis that immune system events involving lymphocytes are necessary for RGC cell death and optic nerve axon loss in glaucoma. This project will determine whether specific populations of lymphocytes are required for RGC death in glaucoma. Based on findings from this study, therapies might eventually be designed to modulate the immune system in order to prevent vision loss and blindness in glaucoma patients.

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Robert W. Nickells, PhD
University of Wisconsin, Madison, Wisconsin

Dr. Henry A. Sutro Family Grant for Research

Project: Purinergic Signaling of Neuroinflammatory Glial Responses in a Model of Optic Nerve Damage

Summary: The central nervous system (CNS) is made up of neuronal cells and support cells, called glia. Whenever there is damage to the CNS, such as in the retina during glaucoma, nerve cells die and glial cells change their behavior in a process called activation. Although glial activation may have short-term benefits, there is consensus that in the long-term, these cells may contribute to the pathology of damaged neurons in glaucoma. Currently, we know that glia become activated in glaucoma, but we do not know by what process. More and more evidence from other parts of the brain suggest that a molecule called ATP is part of the signaling mechanism where damaged neurons tell the glia that they are in distress. We have preliminary evidence that this is also true in the retina after damage to the optic nerve. This proposal is aimed at determining if dying neurons in the retina (ganglion cells) signal to the retinal glia by releasing ATP through specialized channels made up of a protein called Pannexin1. An increased understanding of how the neurons and glia communicate in glaucoma should lead to new developments on how to "tame" the glia into a non-pathologic role, thus increasing the potential for greater preservation of sight.

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Colm O’Brien, MD, FRCS
Mater Misericordiae University Hospital, Dublin, Ireland

Project: Caveolins, Calcium Signalling and Fibrosis of Lamina Cribrosa Cells in Glaucoma

Funding provided by a grant from The Alcon Foundation

Summary: Glaucoma is the second most common cause of vision loss and blindness in the world. Patients with glaucoma present at the clinic with loss of peripheral vision and eye pressure often above normal levels causing compression and damage in a part of the optic nerve called the lamina cribrosa (situated at the back of the eye). We hope to determine if proteins present in lamina cribrosa of glaucoma patients differ to those found in people who do not have the disease; as these proteins may contribute to disease progression. We are interested in three classes of proteins; one which is responsible for the hardening of the cells and their surrounding environment (these are known as fibrotic proteins) in glaucoma and the other which regulates the level of calcium entering and exiting cells. We hypothesise that a third protein group, the caveolin scaffolding proteins, may provide a link between fibrosis and calcium levels and may be responsible for their disregulation in glaucoma. It is our hope that the long-term outcome of this project will be a strategy for relieving the disease burden for sufferers of glaucoma.

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Joshua D. Stein, MD, MS
W.K. Kellogg Eye Center, University of Michigan, Ann Arbor, Michigan

Funding provided by the Glaucoma Research Foundation Board of Directors

Project: A Dynamic, Personalized Glaucoma Monitoring Decision Support Tool

Summary: Our goal is to develop a powerful new type of glaucoma decision support tool to help eye doctors quickly and effectively identify which glaucoma patients are at high risk of getting worse and prevent them from losing more vision. Key features of this innovative technology are that it (1) learns more and more about the stability of the patient's glaucoma with every measurement of eye pressure or visual field, (2) can be personalized to identify the optimal frequency of testing for each individual patient, and (3) would suggest an eye pressure level specific for that particular patient that the care provider would use in the process of recommending treatment. Preliminary results from an early version of this technology demonstrate that it is capable of identifying patients whose glaucoma is getting worse 57% sooner than existing approaches and it is able to significantly reduce the number of eye pressure and visual field measurements required to check for glaucoma worsening. This grant will enable us to advance and expand our technology so that it (1) determines for each patient the ideal level of eye pressure, and (2) guides eye doctors about how frequently each patient should undergo various glaucoma tests like checking eye pressure or undergoing visual field testing. With Glaucoma Research Foundation support, we plan to create this new methodology for a glaucoma decision support tool and further test it so that it will soon be ready to help eye doctors prevent their patients with glaucoma from getting worse.

Last reviewed on October 29, 2017

This article appeared in the May 2014 issue of Gleams.

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