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2017 Research Grants

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

To date, we have awarded more than 200 grants to explore new ideas in glaucoma research. Known as “Shaffer Grants for Innovative Glaucoma Research” in honor of GRF founder Robert N. Shaffer, MD, the Shaffer Grants continue our longstanding commitment to one-year incubation grants to explore novel and promising ideas in the study of glaucoma.

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.

The 2017 research grants are made possible through generous philanthropic support including leadership gifts from The Frank Stein and Paul S. May Grants for Innovative Research, The Alcon Foundation, the Dr. Henry A. Sutro Family Grant for Research, Dr. James and Elizabeth Wise, and The Dr. Miriam Yelsky Memorial Research Grant. Following is a summary of projects we are currently funding.


The 2017 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


Adriana Di Polo, PhD

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University of Montreal

Project: Regeneration of Retinal Ganglion Cell Dendrites: Stimulating Connections to Restore Vision in Glaucoma

Summary: Loss of vision in glaucoma results from the irreversible death of retinal ganglion cells (RGC). Dendrites are exquisitely delicate branches that emerge from the RGC bodies to establish connections with other retinal neurons via highly specialized structures known as synapses. As such, dendrites and synapses are indispensable for successful cell-to-cell communication and visual neurotransmission. An important observation in recent years is that dendrite retraction and synapse loss are one of the earliest pathological responses of RGCs in glaucoma. Indeed, dendritic arbor shrinkage and synapse disassembly have been reported prior to RGC soma or axon death and lead to substantial visual deficits. In this project, we plan to address a critical question: can RGC dendrites regenerate once they have retracted? This is an important issue because individuals with glaucoma do not experience noticeable symptoms until vision loss has begun, a time when there is already tangible RGC loss. We recently identified a highly conserved signaling pathway triggered by the mammalian target of rapamycin (mTOR) kinase as a critical regulator of RGC dendritic structure and function after axonal damage. We plan to test the hypothesis that hormone and/or growth factor-mediated activation of mTOR will stimulate dendrite regeneration and the re-establishment of functional synaptic connections in a model of ocular hypertension glaucoma. The identification of regenerative strategies to restore retinal circuit connectivity will have significant implications to improve neurotransmission, neuronal viability, and visual outcomes in glaucoma.


Markus H. Kuehn, PhD

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The University of Iowa

Project: A New Look at the Role of Microglia in Glaucoma

Summary: The retina and the optic nerve are populated by microglia, a cell type supporting neurons. In glaucoma, activation of these cells is known to result in the production of toxic molecules that lead to neuronal destruction. However, our preliminary data suggest that suppressing the activity of these cells may not be a beneficial therapeutic strategy. Mice with a genetic mechanism to avoid microglial activity develop more retinal damage than control animals with normal microglial function. We propose that the response of microglia to glaucoma damage may have two stages. There is clear evidence that activity of microglia can induce damage in glaucoma, but we propose that this is only true in late-stage disease and that during the early stages of the disease microglia exert a protective effect. Our studies will use mice to test this in the living eye. We will also determine the level of pro-inflammatory cytokines during this process.


The 2017 Shaffer Grants for Innovative Glaucoma Research


John G. Flanagan, OD, PhD

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University of California Berkeley
Funded by Dr. James and Elizabeth Wise

Project: The Role of Lipoxins in Neuroprotection: A Pathway to Understanding Glaucoma

Summary: Glaucoma is a leading cause of blindness and is associated with degeneration of nerves in the retina of the eye. We have discovered that in the normal eye small molecules called lipoxins are released by cells that support and maintain the nerves. Under stress, as happens in glaucoma, these cells appear to stop producing enough of the neuroprotective lipoxins and the neural cells and their axons start to die. We propose to study the role of lipoxins in protecting the nerves of the eye and how they might be involved in the development of glaucoma. To do this we will use a newly developed rodent model that enables the pressure in the eye to be moderately raised over several months. We will also use specially bred mice that are unable to normally use the lipoxin molecules. This will allow us to understand the pathways and mechanisms by which lipoxins can protect the eye, and potentially develop new approaches to the treatment of glaucoma.


Brad Fortune, OD, PhD

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Devers Eye Institute, Portland, OR
The Dr. Miriam Yelsky Memorial Research Grant

Project: Axonal Transport of Mitochondria: Developing an In Vivo Imaging Assay for Glaucoma Research

Summary: Despite astounding recent advances in technological capabilities that enable earlier and more accurate diagnosis of glaucoma, the fundamental events that lead to progressive axon degeneration in glaucoma remain incompletely understood. Thus, even when glaucoma is accurately diagnosed at an early stage, there is still a significant risk for progressive loss of vision, which can be severe in some cases despite successful treatment to lower intraocular pressure. A fuller understanding of the sequence of physiological events that lead to axon damage should provide new targets for both diagnostic technology and therapeutic intervention to be applied during a stage when axons are susceptible, prior to the stages of irreversible degeneration upon which current diagnostic paradigms are based. In this project, we plan to develop an assay of axon transport of mitochondria that can be applied in the living eye to study early pathological events in experimental models of glaucoma. Mitochondria are the motile power plants that supply the fundamental source of energy all along each axon for maintenance of its basic functions, most importantly, conduction of electrical signals to the brain. Evidence suggests that abnormalities of mitochondrial function and transport are among the earliest events after axon injury. There is even evidence from clinical studies suggesting that human beings with better mitochondrial function are less susceptible to glaucoma. Thus, having a reliable assay of mitochondrial transport will be beneficial for future studies to investigate the role of this critical function in the early sequence of glaucomatous axon damage.


Alan L. Robin, MD

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University of Maryland School of Medicine
Funded by the Glaucoma Research Foundation Board of Directors

Project: Meducation: A Randomized Controlled Trial of an Online Educational Video Intervention to Improve Technique and Adherence to Glaucoma Eye Drops

Summary: Glaucoma patients rarely report receiving instruction on eye drop technique from their doctors, and doctors have little time to instruct patients on eye drop technique. A short educational video that can be watched online at home or on mobile devices may help patients learn correct eye drop technique more easily. This study will be the first randomized trial of an educational video for improving eye drop technique. The Meducation® eye drop technique video from Polyglot Systems instructs patients on all the critical steps of proper eye drop technique in easily understandable language with animations to demonstrate each step. This project will be significant because patients who successfully learn better eye drop technique can have a greatly improved chance of performing the crucial skill of eye drop instillation correctly, without added burden to overworked clinicians. By learning better eye drop technique, patients can avoid vision loss and blindness, as well as painful medication side effects and eye infections from contaminated eye drop bottles. The video is easy to disseminate to patients nationwide and does not take any clinician time to deliver.


Gulgun Tezel, MD

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Columbia University, New York, NY
Dr. Henry A. Sutro Family Grant for Research

Project: Autophagy in Neurodegeneration and Neuroinflammation in Glaucoma

Summary: Glaucoma is a leading cause of blindness affecting millions of Americans. However, current treatment strategies are not sufficient to prevent progressive injury to specific nerve cells and continuous loss of visual function. To better understand and treat this blinding disease, our proposed project specifically aims to determine the disease-causing importance of a specific molecular process (named autophagy) in experimental glaucoma models. For this purpose, we will model glaucoma in specific mouse strains lacking the activity of specific molecules in nerve cells or glia (another important cell type that are adjacent to nerve cells and play diverse roles to support nerve cells or contribute to inflammatory nerve injury) and analyze specific responses of neurons and glia using up-to-date analysis techniques. We expect that this project will enable us to value whether therapeutic manipulation of autophagy provides protection against nerve inflammation and injury in glaucoma. The new information should help develop new treatment possibilities for patients suffering from this disease.


Carol B. Toris, PhD

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Case Western Reserve University, Cleveland, OH
Funded by The Alcon Foundation

Project: Lowering of IOP by Improved Drainage through the Ciliary Muscle

Summary: This research project seeks to understand how movement of the muscle within the fluid drainage pathway of the eye (ciliary muscle) affects the eye pressure. This muscle has two functions: it allows us to focus our vision on near or far objects, and it is a pathway for fluid drainage from the eye (uveoscleral outflow). We can change our focus at will, which means we have conscious control over this muscle. The more the muscle is moved, the more fluid is squeezed out of the eye and the lower the eye pressure. This suggests that eye exercises may be an indirect way to help treat the high pressure often seen in glaucoma. This idea will be tested in adult volunteers. For one aim of the study we will examine in young adult volunteers how much the eye pressure changes when staring at a distance, when focusing up close, or when alternating between near and far vision. For the second aim, we will study how older adults who have trouble focusing up close (presbyopia) also have difficulty changing their eye pressure. Finally, results from young adults and older adults will be compared to see how aging affects fluid drainage and eye pressure. The objective of this project is to better understand how the eye drains fluid and controls eye pressure.


Tara Tovar-Vidales, MS, PhD

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University of North Texas Health Science Center, Fort Worth, TX
Funded by The Alcon Foundation

Project: Role of microRNAs (miRNAs) in Pathologic Fibrosis in the Glaucomatous Optic Nerve Head

Summary: In glaucoma there is extracellular matrix (ECM) remodeling of the optic nerve head (ONH). The ONH astrocytes and lamina cribrosa cells synthesize ECM proteins to support the ONH. However, in glaucoma, these cells cause detrimental changes to the ONH. We want to understand the regulation involved in glaucomatous ECM remodeling of the ONH. Specifically, we will examine the expression of miRNAs in normal and glaucomatous ONH astrocytes and lamina cribrosa cells to determine which miRNAs are associated with glaucoma. Additionally, we will examine the expression of miRNAs in astrocyte and lamina cribrosa cells with and without TGF-β2 treatment to determine if the profibrotic cytokine TGF-β2 differentially expresses miRNAs. This project will identify profibrotic and antifibrotic miRNAs that regulate ECM and ECM related proteins in the glaucomatous ONH and may provide a novel therapy to treat glaucoma patients.

Last reviewed on May 03, 2017

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