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2020 Research Grants

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

To date, we have awarded more than 250 grants to explore new ideas in glaucoma research.

Known as “Shaffer Grants for Innovative Glaucoma Research” in honor of GRF founder Dr. Robert N. Shaffer, 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 $50,000.

The 2020 Shaffer Grants for Innovative Glaucoma Research are made possible through generous philanthropic support including leadership gifts from the Frank Stein and Paul S. May Grants for Innovative Glaucoma Research, Akorn, Inc. and Team Akorn, the Edward Joseph Daly 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 2020 Shaffer Grants for Innovative Glaucoma Research


Steven Bassnett, PhD

Washington University School of Medicine
Funded by The Dr. Miriam Yelsky Memorial Research Grant

Project: Role of LOXL1 Propeptide Aggregation in Pseudoexfoliation Glaucoma

Summary: Pseudoexfoliation (PEX) syndrome is the most common identifiable cause of glaucoma, afflicting millions of people worldwide. In patients with PEX syndrome, white, powdery material accumulates on the front surface of the eye lens. Under the microscope, the powdery aggregates can be seen to consist of tangled fibrils. Contraction of the pupil dislodges the PEX material and abrades the inner lining of the iris, causing release of pigment. The combination of PEX material and pigment granules can block the drainage pathways of the eye. As a result, many PEX patients experience unusually high pressure within the eye and nearly half go on to develop PEX glaucoma, a challenging condition to treat clinically because it is resistant to medical therapy. Genetic studies have suggested that inherited variations in a gene called LOXL1 are closely associated with the risk of developing PEX syndrome, but the precise link between the presence of genetic variants and the disease mechanism remains obscure. We will test the hypothesis that aggregation of the LOXL1 propeptide is an initiating event in PEX fibril formation. This will provide important insights into the etiology of PEX glaucoma.


Stewart Bloomfield, PhD

State University of New York College of Optometry
Funded by the Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Project: Retinal Gap Junctions Form Novel Targets for Neuroprotective Therapy in Glaucoma

Summary: The use of IOP-lowering drugs, the current mainstay treatment for glaucoma, is often insufficient to prevent progressive visual loss in patients. Therefore, recent work on potential glaucoma treatments have shifted to assessment of neuroprotective strategies to promote neuronal survivability and thereby preserve visual function. Our strategy is to determine the mechanism(s) responsible for secondary cell loss in glaucoma to create novel preventive treatments. Our experimental program will study a novel mechanism for cell loss in glaucoma, so as to specify targets for innovative treatments to preserve cell health and visual function. While our project will focus on glaucoma, our results should inform potential treatments of other neurodegenerative diseases of the retina, such as retinitis pigmentosa and ischemic retinopathy, as well as other degenerative brain insults, such as stroke.


Alex Huang, MD, PhD

Doheny Eye Institute
Funded by Dr. James and Elizabeth Wise

Project: Investigating Subconjuctival Lymphatics for the Treatment of Glaucoma and Eye Disorders

Summary: In order to have a successful glaucoma surgery, intraocular fluid must both enter into and exit subconjunctival blebs. This latter phenomenon is much less understood. Thus, this proposal studies the biology of subconjunctival fluid outflow in order to develop strategies to enhance it for improved glaucoma surgical outcomes. We start by evaluating a long‐standing but unproven hypothesis that lymphatics drain the subconjunctival space and blebs. We utilize imaging methods which can isolate fluid outflow pathways from blebs for exact structural and molecular identification. Then, we develop methods to manipulate bleb outflow pathways using protein growth factors. We hypothesize that growing more lymphatics into subconjunctival blebs can help glaucoma surgeries akin to building rivers past a dam to move water past the obstruction. With these tools in hand we hope to better understand glaucoma surgeries, develop tools to improve them, and in so doing preserve vision with less patient reliance upon daily glaucoma drops.


Tatjana Jakobs, MD

Schepens Eye Research Institute
Funded by the Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Project: The Transcription Factor Runx1 as a Novel Mediator of Astrocyte Reactivity in the Optic Nerve

Summary: In glaucoma, the retinal ganglion cells degenerate and die, which causes the characteristic vision defects in this disease. At the moment, lowering the intraocular pressure is the therapy of choice but this is not effective in all cases. A neuroprotective approach that directly prevents ganglion cell death and that could be combined with pressure-lowering drugs would be welcome. The retina and optic nerve contain supporting cells (astrocytes) that normally carry out important tasks to help ganglion cell function. In case of injury, such as an elevation of intraocular pressure, astrocytes become reactive. This is at least initially a protective response that aims to save retinal ganglion cells and their axons from degeneration. We have studied the molecular mechanisms of astrocyte reactivity and identified a transcription factor (Runx1) that is up-regulated in reactive astrocytes. Our hypothesis is that Runx1 directs the expression of other genes in the astrocytes that support ganglion cell survival. We want to identify these genes and the proteins they encode. Ultimately, the goal is to provide neuroprotective factors therapeutically in glaucoma.


Rachel Kuchtey, MD, PhD

Vanderbilt Eye Institute

Project: Investigation of Ocular Biomechanical Defects in Mice with Microfibril and Elastic Fiber Defects

Summary: Age-related changes in the stiffness of ocular tissue have been well recognized in glaucoma, though how these alterations take place is not fully understood. Two challenges are lack of good models and sophisticated tools to measure tissue mechanical properties. We and others have reported causative genetic mutations in ADAMTS10 and ADAMTS17 in dogs with inherited glaucoma. Because both genes encode microfibril-associated proteins, we have focused on well-characterized and well-established mouse models with microfibril defects caused by Fbn1 mutations. Fbn1 mutant mice have multi-organ biomechanical defects, and we recently reported ocular findings related to glaucoma in those mice. We believe those mice could be a good model to study ocular biomechanical properties. We further hypothesize that disruption of an additional key component of elastic fibers would result in more severe ocular biomechanical defects. We will use Atomic Force Microscopy to address the other challenge, lack of tools for measuring small tissues, such as mouse aqueous outflow and optic nerve.


Herbert Lachman, MD

Albert Einstein College of Medicine
Funded by the Edward Joseph Daly Foundation

Project: Gene Expression Profiling in Trabecular Meshwork Cells derived from Induced Pluripotent Stem Cells made from Patients with Lowe Syndrome, a Genetic Disorder that causes Cataracts and Glaucoma

Summary: Glaucoma is one of the most common causes of blindness. Although researchers have been studying its underlying biological basis for decades, blindness still occurs far too often. New scientific breakthroughs have provided unique opportunities to study the disorder from a fresh perspective, with the ultimate goal of discovering novel therapies. One breakthrough is the development of induced pluripotent stem cell (iPSC) technology, which allows investigators to turn white blood cells or skin cells into virtually any other cell type in the body - including eye tissue. Another breakthrough is the ability to analyze the expression pattern of every gene in a cell, which provides a window into the function of that cell, and how that function goes awry in disease. In this proposal, we plan on generating eye tissue from iPSCs made from individuals with Lowe Syndrome, a rare genetic disorder that leads to congenital cataracts and glaucoma. We will study the gene expression pattern in eye tissue derived from the iPSCs to find novel pathways involved in the development of glaucoma.


Matthew B. Veldman, PhD

Medical College of Wisconsin
Funded through a special gift from Akorn, Inc. and their employees

Project: Zebrafish Retinal Ganglion Cell Survival in the Context of Pro-Apoptotic Bax Signaling

Summary: In glaucoma, elevated internal eye pressure or other events such as inflammation cause damage to the nerve sending signals from the eye to the brain. Following this injury, the cells that directly connect the eye to the brain die resulting in loss of vision. This is also true in non-human, mammalian models of the disease, however in animals such as fish the injured cells survive, and vision recovers. How these animals recover after nerve injury is not well understood, but the genes and proteins involved are highly evolutionarily conserved with mammals and people. Therefore, it is likely that mechanisms supporting cell survival and regeneration in fish will be translatable to glaucoma patients and might suggest therapeutic targets. Cell death in glaucoma models and likely patients is dependent upon the protein BAX which is part of the programed cell death pathway. This gene and pathway are conserved in fish, yet injured cells do not die following injury. The goal of this project is to establish a system for studying this gene and pathway in the eye of the zebrafish model organism and determine how it remains turned off following nerve injury.


Trent A. Watkins, PhD

Baylor College of Medicine

Project: Highly Parallel Assessment of RGC Regenerative and Neuroprotective Targets

Summary: The loss of vision in glaucoma is a consequence of the disconnection of the nerve fibers that connect neurons in the eye with neurons in the brain. Our lab is developing a system to substantially increase our capacity to evaluate potential therapeutic interventions to preserve and repair these connections. Our proposed system tackles, in parallel, three interrelated biological processes that contribute to irreversible vision loss in glaucoma: (1) the degeneration, or “die-back,” of optic nerve fibers, such that they are no longer available to deliver visual information to the brain; (2) the failure of these fibers, unlike those of peripheral nerves, to regenerate and re-establish functional communication; and (3) the tendency of diseased retinal neurons to commit cellular suicide, precluding any hope for later repair. Current evidence suggests that successfully enable preservation and restoration of vision will require a combination of interventions that influence each of these processes. We propose that utilizing the remarkable sensitivity of molecular barcoding will allow for testing multiple candidates in parallel and in combination for their impacts on preserving and restoring connections between the retina and the brain.

Last reviewed on June 04, 2020

This article appeared in the May 2020 issue of Gleams.


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