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Research Results

Each year the Glaucoma Research Foundation awards Shaffer Grants to worthy investigators with innovative ideas. On this page are posted research results from previous years.

Included are final results from recent research projects funded by Glaucoma Research Foundation with downloadable posters (PDF) and summaries of findings.

A clear research focus and strong leadership from an expert board of Scientific Advisors is key to the success of our Shaffer Grants for Innovative Glaucoma Research.

Some of the most important discoveries in scientific research come from an investigator with a new, untested idea who needs funding to explore a creative project. Shaffer Grants provide seed money for pilot research projects that hold promise and explore new ideas.

Following are annual research grants awarded in recent years. Since 2019, all one-year grants are in the amount of $50,000.

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

Project 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

Project 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

Project 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

Project 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

Project 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

Project 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

Project 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

Project 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.

The 2019 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


Daniel M. Lipinski, PhD
Medical College of Wisconsin
Project: Development of rAAV Vector Technologies to Facilitate Topical Gene Delivery to the Cornea

Download Dr. Lipinski's final project research poster (PDF) »

Final Report Summary: New genetic material can be delivered to cells of the cornea via injection of a viral vector into in to the front chamber of the eye. Whilst this method is largely effective, it substantially increases the risk of patients developing complications, including eye infections, such as endophthalmitis or uveitis. Furthermore, injecting extra fluid into the eye leads to a transient, but dramatic, spike in intraocular pressure that may potentially accelerate vision loss in patients with glaucoma. In this project we explored an alternative gene delivery approach wherein the virus vector was attached to the inside of a contact lens, rather than being injected, and then the contact lens placed on the front of the eye for a brief period (30 minutes). Our main findings were that virus vectors immobilized on to a contact lens remain active, they stay in close contact with the cornea for long periods of time, and are able to penetrate the cornea and successfully deliver new genetic material effectively. These findings represent a positive step towards the development of a non-invasive gene therapy treatment for glaucoma.


Biraj Mahato, PhD
University of North Texas Health Science Center
Project: Chemically Reprogrammed Retinal Ganglion Cell Therapy to Treat Glaucomatous Neuropathy

Project Summary: Retinal ganglion cells (RGCs) are the neurons that transmit light signal from the eye to the brain so that we can see. Even when rest of the visual system is healthy, if RGCs are dead or dysfunctional, vision is impossible. RGCs are primarily damaged in glaucoma with its attendant elevated eye pressure and once damaged they fail to regenerate, leading to irreversible blindness. Stem cells are promising tools to replace RGCs and have garnered considerable excitement. However, the protocol to obtain such cells are cumbersome and time consuming. There are many hurdles and challenges that have yet to be overcome, leading scientists to search for alternate strategies. In an exciting discovery we have identified a set of five small molecules that can reprogram human skin fibroblasts to retinal ganglion cells. Our method demonstrates a safe, effective, and efficient source of RGC replacement cells to restore vision, without the use of embryonic or other pluripotent stem cells. In depth molecular analysis of chemically converted RGCs and exploring their prospective function in a rodent model carries extraordinary translational potential for millions of visually impaired glaucoma patients worldwide.

The 2019 Shaffer Grants for Innovative Glaucoma Research


Steven Barnes, PhD
Doheny Eye Institute
Funded by Roberta and Robert H. Feldman
Project: Functional Resilience of Retinal Ganglion Cells During Mitochondrial Dysfunction

Download Dr. Barnes's final project research poster (PDF) »

Final Report Summary: The production of energy in retinal ganglion cells is accompanied by metabolic byproducts, many of which are damaging to cellular function. The issue of how these byproducts modulate the excitability of retinal ganglion cells (RGCs) bears heavily on the development, impact, and early detection of optic neuropathies, including glaucoma. Our goals in undertaking this project were to test novel hypotheses about how the metabolic milieu of RGCs affects their electrical signaling of visual information. Our investigations identified the characteristics and biophysical origins of changes to the physiological properties of RGCs due to oxidizing byproducts in the retina. This new knowledge will increase understanding of both normal retinal physiology as well as the pathophysiology of glaucoma. Our novel observations support an emerging model of early stages of glaucoma where increases in oxidizing chemical species during energy production, but not necessarily bioenergetic failure, leads to preferential degeneration of certain subtypes of retinal ganglion cells, resulting in loss of specific aspects of visual capabilities.


Adnan Dibas, PhD
North Texas Eye Research Institute
Funded by the Edward Joseph Daly Foundation
Project: Endothelin Converting Enzyme Knockdown is Neuroprotective in Glaucomatous Neuropathy

Project Summary: Very little is known about how and why the optic nerve is progressively damaged in glaucoma. Conditions known to cause glaucoma such as elevated intraocular pressure (IOP), hypoxia, and ischemia were found to be associated with changes in the expression of aquaporin water channels in non-ocular tissues (e.g. brain, neurons, and muscle). Conditions known to cause glaucoma such as elevated IOP are associated with increased small proteins known as endothelins. Data obtained in the current study suggests that elevation of IOP in rats resulted in the activation of endothelin-producing enzymes known as ECE. Therefore, reduction of ECE activities may be a novel therapeutic in the treatment of glaucoma. Currently glaucoma medication involves only pressure lowering medication; however, vision loss continues. Therefore, the identification of additional mechanisms that continue to promote vision loss will assist in the development of combination therapy of lowering pressure and preventing vision loss in glaucoma.


Pierre Mattar, MSc, PhD
Ottawa Hospital Research Institute
Funded by Carolyn and Richard Sloane
Project: Programming and Reprogramming for Retinal Ganglion Cell Replacement Therapy

Final Report Summary: Although glaucoma is frequently treatable with medication or surgery, a large proportion of afflicted individuals are diagnosed too late to prevent the death of key retinal neurons, which are called retinal ganglion cells (RGCs). As RGCs are the only neurons that transmit information from the eye to the brain, their loss results in permanent vision impairment. Although RGCs cannot be naturally regenerated, they can be produced artificially from retinal stem cell cultures. Stem cell cultures potentially offer the promise of recovery for vision loss. However, in order to bring this approach to the clinic, we will need to greatly improve our ability to produce these cells efficiently. We have been developing an approach that will allow RGC production to be enhanced. We have identified several genetic modifications that enhance RGC production, using genes that have been shown to perform this function during the natural development of the eye. Applying these genetic modifications to retinal stem cell models is expected to facilitate the production and transplantation of RGCs for glaucoma therapy.


Lauren Katie Wareham, PhD
Vanderbilt University Medical Center
Funded by Dr. James and Elizabeth Wise
Project: Investigating the Role of the NO-GC-1-cGMP Signaling Pathway in Glaucoma

Project Summary: The GC1 murine model of glaucoma aligns well with the pathophysiology seen in primary open angle glaucoma patients; the disease progresses with age, and mice have moderately elevated IOP, leading to degeneration of the optic nerve. This mouse model is novel, and the work completed in this proposal has already highlighted significant transcriptional changes that may underlie the pathology observed in these mice, and thus may eventually translate to human subjects. In the short term, investigating further the role of cGMP in glaucoma will highlight pertinent pathways in glaucoma pathology that may be targeted with pharmaceuticals to delay progression of the disease. We have already established that an FDA-approved drug, tadalafil, prevents neurodegeneration in two mouse models of glaucoma. We now aim to investigate the mechanisms behind this finding in order to highlight additional downstream drug targets. We are attempting to undertake the first step in this vision; by augmenting inflammatory pathways with drugs in murine chow, we aim to investigate whether cGMP neuroprotection is dependent on inflammatory modulation, and whether this leads to increased degeneration/neuroprotection of retinal ganglion cells. In the long term, this work furthers the exciting finding that modulating cGMP signaling increases retinal ganglion cell survival. The RNA sequencing analysis will provide a wealth of data, which will be published and an open resource for mining, which may highlight other relevant gene targets for future investigation by us and other groups.

Pete Williams in the lab

Pete A. Williams, PhD
Karolinska Institutet
Funded by the Dr. Henry A. Sutro Family Grant for Research
Project: Targeting Neuronal Mitochondria for Neuroprotection in Glaucoma

Download Dr. Williams's final project research poster (PDF) »

Final Report Summary: Current glaucoma treatment strategies only target IOP, the principal treatable risk factor. Neuroprotective treatments for glaucoma are of great therapeutic need. We have recently discovered a role for nicotinamide (a form of vitamin B3) in protecting the optic nerve in glaucoma by targeting these metabolic processes that change in the retina early during glaucoma. Nicotinamide is well tolerated, inexpensive, and robustly protective and thus may be an ideal therapeutic candidate for human glaucoma patients. To this, recent evidence demonstrate that nicotinamide is low in the sera of primary open angle glaucoma patients and we have been part of a multi-national collaborative group that has demonstrated that oral nicotinamide can increase visual function in existing glaucoma patients. Given nicotinamide’s obvious clinical utility, more research is warranted on understand that exact roles of nicotinamide in retinal ganglion cell and optic nerve health in aging and disease. In this project we have demonstrated that mitochondria rapidly change in morphology during retinal ganglion cell injury at time points prior to gross cell death. In both mouse and rat systems that mimic glaucoma-related insults we report that nicotinamide prevents these early mitochondrial changes and protects from retinal ganglion cell neurodegeneration, extending our knowledge about nicotinamide’s role in glaucoma.


Dr. Williams was awarded the 2021 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

The 2018 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


Padmanabhan Pattabiraman, PhD
Case Western Reserve University
Project: Anti-fibrogenic Matricellular Protein CCN1 as a Novel Therapeutic Target to Lower Intraocular Pressure

Project Summary: Critical barriers in the development of efficient IOP lowering therapies could be overcome if there were a better mechanistic understanding governing ECM homeostasis, TM stiffness and the pathobiological basis of altered ECM deposition in the aqueous humor outflow pathway leading to increased stiffness and outflow resistance. Our research shows that targeting CCN1 can be beneficial in increasing aqueous humor outflow. The data we find indicates that increasing CCN1 expression is able to attenuate the TGFβ2-mediated increase in TM stiffness by lowering pro-fibrogenic activity in the HTM cells caused by TGFβ2. We believe that since the CCN1 lowers the tissue stiffness and attenuates TGFβ2-mediated effects on HTM cells, CCN1 is a therapeutic target to lower IOP.


Giuliano Scarcelli, PhD
University of Maryland
Project: Noncontact Mechanical Mapping of the Optical Nerve Head with Brillouin Microscopy

Download Dr. Scarcelli's final project research poster (PDF) »

Final Report Summary: The mechanism by which elevated IOP levels induce degradation of the optical nerve head (ONH), the initial site of injury in glaucoma, is not yet understood but it is widely suspected that a main culprit is the lack of mechanical balance between IOP-induced strains and the stiffness of ONH and surrounding sclera. However, we do not have viable technology to test the stiffness of the back of the eye. We have developed a potential solution to this need, an all-optical approach to mechanical measurements using Brillouin light scattering. Our technology is already in human clinical trials for transparent ocular tissues (cornea, lens). In this grant we extended the reach of Brillouin microscopy to the back of the eye by using Adaptive Optics (AO). We have demonstrated that our new AO-Brillouin microscope enables imaging opaque tissues such as ONH and sclera, we have validated the instrument to show we can measure the expected mechanical differences at the back of the eye. Thus, this pilot grant provided proof-of-principle for the use of this new technology in glaucoma animal models to measure novel functional/mechanical parameters of the sclera and ONH.

The 2018 Shaffer Grants for Innovative Glaucoma Research


Monica M. Jablonski, PhD
University of Tennessee Health Science Center
Funded by the Edward Joseph Daly Foundation
Project: Extended Release IOP-Lowering Formulation

Download Dr. Jablonski's final project research poster (PDF) »

Final Report Summary: Glaucoma is the leading cause of irreversible blindness in the world, which is projected to affect about 6.3 million Americans by 2050, and intraocular pressure (IOP) is a leading contributor to glaucoma. Our project addresses the major limitations of current glaucoma therapy by advancing a sustained-release IOP-lowering formulation that coordinates multiple targets to normalize IOP. Minimum performance metrics for the novel formulation will position us to move toward clinical trials and eventually to commercialization.


Mary J. Kelley, PhD
Oregon Health & Sciences University
Funded by Dr. James and Elizabeth Wise
Project: Trabecular Meshwork Stem Cells and the Identification of the Laser Factor

Download Dr. Kelley's final project research poster (PDF) »

Final Report Summary: A healthy normally functioning eye is dependent upon a certain number of cells for good vision. The primary risk factor for glaucoma is elevated pressure inside the eye (intraocular pressure). The trabecular meshwork or TM is responsible for controlling this pressure, but with age and glaucoma the TM loses cells and sometimes can no longer perform its regulatory function. Glaucoma can be treated for some limited amount of time with a laser, which will burn holes in the TM, and restore the pressure to normal. Previously, we found that when human cadaver eyes are treated with a laser, there is increased cell division and migration to the areas burned. These laser-treated eyes were put into organ culture with growth medium, and when this medium was later collected, it now had molecules from the cells of the laser-treated eyes and is called “conditioned media”. When this conditioned medium was placed on non-laser treated human cadaver eyes, cell division and migration also increased in these untreated eyes, suggesting that the growth medium contained secreted substances from the laser treated TM cells. Laser-treated cells of the first eye produced a “laser factor” into the medium which increased TM cell division and migration. This project involves the isolation and identification of this factor. If we can identify what this substance is, it can be chemically synthesized and added to eye drops for the patient. Treatment with such eye drops could stimulate the stem cells of the TM in glaucomatous eyes to increase cell division and migrate to the areas needed to restore function to the eye. Our results indicate that a growth factor, PDGFbb, is a molecule important in cell division, and caused the largest amount of increase in cells. However, TNF-alpha and IL-1 seem promising as well, and there may be other factors that are important to this process. Further studies are ongoing on cell migration and on affirming our initial results with cell division.


David Krizaj, PhD
University of Utah
The Dr. Miriam Yelsky Memorial Research Grant
Project: Regulation of Tensile Homeostasis in the Trabecular Meshwork

Download Dr. Krizaj's final project research poster (PDF) »

Final Report Summary: Given that pressure-lowering eye drops are by far the most common treatment for glaucoma it is astounding that we know so little about how the effects of pressure are sensed and transduced in the eye. The project supported by GRF identified and studied new classes of ion channels that are specialized for pressure transduction. Our studies showed why and how pressure is such a potent regulator of ocular physiology and also identified pressure-sensing ion channels as targets for a novel generation of anti-glaucoma drugs. The take-home message is that trabecular meshwork cells, which play the central role in intraocular pressure regulation, exist in the state of “tensile balance” that is maintained by dynamic activation of at least three different pressure sensitive channels. Our results suggest that the loss of pressure regulation in glaucoma may occur in part due to the disturbed balance between these pressure sensors.


Yvonne Ou, MD
University of California, San Francisco
Funded by Roberta and Robert H. Feldman
Project: Ganglion Cell Dysfunction in Glaucoma

Download Dr. Ou's final project research poster (PDF) »

Final Report Summary: Glaucoma is an irreversible blinding disease in which the cells that comprise the optic nerve, the retinal ganglion cells (RGCs), are damaged and die. A major gap in taking care of glaucoma patients is that we do not have an objective test that measures how well the RGCs are functioning. There are actually over 30 types of RGCs, and our laboratory has recently identified specific types of RGCs that are more vulnerable in glaucoma. Taking advantage of this knowledge, we are developing novel methods to assess the function or health of RGCs that are more vulnerable versus more resistant to damage. A more sensitive and objective test of RGC function and health will greatly improve our ability to take care of glaucoma patients and their vision.


Dorota Skowronska-Krawczyk, PhD
University of California, San Diego
Funded by the R. David Sudarsky Charitable Testamentary Trust
Project: Eliminate to Protect

Download Dr. Skowronska-Krawczyk's final project research poster (PDF) »

Final Report Summary: Glaucoma is a group of optic neuropathies characterized by slow, progressive loss of retinal ganglion cells (RGCs), degeneration of the optic nerve and, consequently, loss of vision. Although the main risk factors associated with the development of the disease are elevated intraocular pressure and aging, genetic studies have described a number of loci in the genome that further increase the risk of glaucoma. Our previous work has indicated that upon intraocular pressure elevation RGCs become senescent and affect surrounding cells. In our project, we proposed to remove early senescent RGCs in the glaucomatous eye as a way to protect neighboring RGCs from death. Using mouse model of hypertension in the eye we were able to show that early removal of affected-senescent cells is beneficial for the eye in two ways: i) Fewer ganglion cells are lost in the retina; ii) Remaining cells in the retina are functional and overall visual functions are preserved. Therefore, our project provided a solid foundation for future studies on potential applications of senolytic drugs in glaucoma patients as a way to prevent the glaucoma progression.


Dr. Dorota Skowronska-Krawczyk was awarded the 2020 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.


Trent A. Watkins, PhD
Baylor College of Medicine
Dr. Henry A. Sutro Family Grant for Research
Project: Elucidating the Dynamics of the Neuronal Stress Response in Driving the Death of Retinal Ganglion Cells

Download Dr. Watkins's final project research poster (PDF) »

Final Report Summary: In this study, we have developed a new tool for understanding how the efforts of retinal neurons to repair themselves in glaucoma can ultimately contribute to their demise. Previous research had revealed that one potential means by which vision is lost is through a series of events that results in neuronal suicide. Retinal neurons essential for vision are challenged by disease-related changes, and their efforts to adapt to these challenges include cellular signaling that promotes repair but can also lead to cell death. We have established a tool that allows us to stimulate this signaling at various intensities and patterns to probe how and when it goes from beneficial to detrimental. Our findings so far suggest that modest stimulation may, when combined with other interventions, improve neuronal repair and survival.

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


Adriana Di Polo, PhD
University of Montreal
Project: Regeneration of Retinal Ganglion Cell Dendrites: Stimulating Connections to Restore Vision in Glaucoma

Download Dr. Di Pilo's final project research poster (PDF) »

Final Report Summary: Loss of vision in glaucoma results from the irreversible death of retinal ganglion cells (RGCs). A crucial step towards circuit repair in glaucoma is to promote damaged RGCs to regenerate not only axons, but also dendrites to successfully reconnect with their synaptic partners. In this study, we tested the hypothesis that insulin will stimulate dendrite regeneration and the reestablishment of synaptic connections thus improving survival and function in injured RGCs. Using a range of genetic, pharmacological, imaging, and electrophysiological in vivo approaches, we show that insulin promotes striking RGC dendrite and synapse regeneration in injured RGCs. Importantly, insulin promoted robust neuronal survival and rescued light-triggered retinal responses.

Our study reveals that adult RGCs are endowed with the ability to effectively regenerate dendrites and synapses once they have been lost, and identifies insulin as a powerful strategy to restore dendritic morphology and enhance the function and survival of these neurons. Collectively, our data support the rationale for using insulin and its analogues as proregenerative therapeutic targets to counter progressive RGC neurodegeneration and vision loss in glaucoma. In summary, our findings are innovative and a major scientific advancement in the field.

This work was accepted for publication in the prestigious journal Brain (July 2018 issue).


Dr. Adriana Di Polo was awarded the 2019 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.


Markus H. Kuehn, PhD
The University of Iowa
Project: A New Look at the Role of Microglia in Glaucoma

Project 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. 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. 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
University of California Berkeley
Funded by Dr. James and Elizabeth Wise
Project: The Role of Lipoxins in Neuroprotection: A Pathway to Understanding Glaucoma

Project 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
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

Download Dr. Fortune's final project research poster (PDF) »


Alan L. Robin, MD
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

Download Dr. Robin's final project research poster (PDF) »

Final Report Summary: A short educational video can significantly improve glaucoma patients’ short-term self-efficacy and eye drop technique. Videos may provide an inexpensive, convenient way to deliver eye drop technique education in any provider’s office or online.

This work was accepted for publication in the journal Patient Education and Counseling (December 2018 issue).


Gulgun Tezel, MD
Columbia University, New York, NY
Dr. Henry A. Sutro Family Grant for Research
Project: Autophagy in Neurodegeneration and Neuroinflammation in Glaucoma

Download Dr. Tezel's final project research poster (PDF) »

Final Report Summary: Glaucoma is a leading cause of blindness affecting millions of Americans. However, current treatment strategies are not sufficient to prevent disease progression. We expect that by improving the molecular understanding of autophagy that impacts both retinal ganglion cell (RGC) survival/axon integrity and glia-driven inflammation, this project will provide translational implications for development of neuroprotective and immunomodulatory treatments for glaucoma.


Carol B. Toris, PhD
Case Western Reserve University, Cleveland, OH
Funded by The Alcon Foundation
Project: Lowering of IOP by Improved Drainage through the Ciliary Muscle

Download Dr. Toris's final project research poster (PDF) »

Final Report Summary: Our proposed research sought 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 change our focus to clearly see 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. Our study supported the idea that the more we move the muscle (change our focus), the more fluid is squeezed out of the eye and the lower the eye pressure. This idea was tested in three groups of adult volunteers aged 20-25 years, 40-49 years and 60-69 years. We tested how much the eye pressure changed when staring at a distance, when focusing up close, or when alternating between near and far vision. This was done for 10 minutes per test with a 20-minute rest in between tests. The results showed that alternating accommodation lowered eye pressure significantly and surprisingly the age of the person did not make a difference. This project helped to better understand how the ciliary muscle drains eye fluid and controls eye pressure. In a future study we will investigate glaucoma patients with high pressure with the ultimate goal of finding better treatments for this blinding disease.


Tara Tovar-Vidales, MS, PhD
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

Download Dr. Tovar-Vidales's final project research poster (PDF) »

Final Report 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 the detrimental changes to the ONH. We want to understand the regulation involved in glaucomatous ECM remodeling of the ONH. In this study, we examined microRNAs (miRNAs) which are small molecules that silence gene expression. In this project, we treated human astrocytes and lamina cribrosa cells with or without the profibrotic cytokine TGFβ2 to compare miRNA profiles. Our results identified profibrotic and anti-fibrotic miRNAs that are dysregulated in both astrocytes and lamina cribrosa cells with TGFβ2 treatment. We also observed by using small molecules that act as miRNA mimics, we can block the effects of TGFβ2 induced ECM expression or ECM related proteins that are associated with glaucoma. We believe miRNAs are of interest to help us understand the cellular mechanisms that occur in the glaucomatous ONH and may provide a novel therapy to treat glaucoma patients.

The 2016 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


David T. Stark, MD, PhD
Stein Eye Institute, David Geffen School of Medicine at UCLA, Los Angeles, CA
Project: Endocannabinoids in Retinal Ganglion Cell Regeneration

Download Dr. Stark's final project research poster (PDF) »

Final Report Summary: Many optic nerve diseases result in permanent loss of vision. This occurs in part because the intrinsic growth capacity of retinal ganglion cells rapidly declines after birth, and injured central nervous system axons fail to regenerate. The scientific community has learned a great deal about molecular signals that can support regeneration of damaged neural connections, but there is an urgent need to identify as many pro-regenerative signals as possible because it is not clear which of these might actually translate to use in patients.

Generous support from the Glaucoma Research Foundation allowed us to develop a strategy to comprehensively assess an entire class of biomolecules called lipids for differences that occur during optic nerve regeneration. We hope to use this approach to identify candidate molecules that might represent previously unknown pro-growth signals.

Findings from this research study were published in the January 2018 issue of IOVS (Investigative Ophthalmology & Visual Science), "Optic Nerve Regeneration After Crush Remodels the Injury Site: Molecular Insights From Imaging Mass Spectrometry."


Frank Talke, PhD
University of California, San Diego
Project: Development of an Optical-based Intraocular Pressure Sensor

Download Dr. Talke's final project research poster (PDF) »

Final Report Summary: We have developed an intraocular pressure sensor based on the principle of interferometry. The sensor is comprised of a diaphragm and a glass substrate. By directing monochromatic light towards the active sensing region and applying pressure, one can observe interference fringes as the diaphragm deflects. Using the principle of interferometry, we were able to back calculate pressure using the images captured by a camera. From our studies, we have found the best results using silicon nitride as the diaphragm material. The sensor read-out can be further optimized by coating a thin layer of silicon nitride onto the glass substrate. In order to further demonstrate proof of concept, our sensor was also tested ex-vivo using a rabbit eye model. Thus far, we have achieved 0.8 mmHg resolution. Our results show that the sensor response is repeatable and agree with mathematical models.

The 2016 Shaffer Grants for Innovative Glaucoma Research


Kevin Park, PhD
University of Miami Miller School of Medicine, Miami, FL
Funded by The Melza M. and Frank Theodore Barr Foundation, Inc.
Project: Axon-astroglial Interaction and its Effects on Optic Nerve Repair

Download Dr. Park's final project research poster (PDF) »

Final Report Summary In glaucoma, the optic nerve which sends visual information from eye to brain gets damaged. Once damaged, the optic nerve does not regrow back to the brain, resulting in permanent blindness. Therefore, to restore visual function in glaucoma patients, it might be necessary to promote injured optic nerves to regenerate and reconnect to their original targets.

In the last several years, researchers have identified gene therapies that can promote optic nerve regeneration. However, there is a still major problem. Optic nerves are mostly incapable of growing straight back to the brain, and often fail to reach the brain. In our research, we seek to understand the cellular and genetic factors that prevent these nerves to correctly find their targets. Towards this goal, we first discovered that optic nerves regenerate physically on the surface of astrocytes which are the support cells in the optic nerve. Therefore, we reveal that optic nerve regeneration and navigation are in fact shaped by astrocytes.

Second, we discovered that certain genes, namely Ncad expressed in the astrocytes, are important for optic nerve interaction with astrocytes, and for optic nerve regeneration. Our study identified the key cellular and genetic players that shape optic nerve regeneration and navigation. Ultimately, our research will help elucidate factors that prevent proper optic nerve regeneration and guidance, and to find strategies that promote reconnection of damaged optic nerves and restore visual functions following optic nerve damage.


Ian Pitha, MD, PhD
Johns Hopkins University, Wilmer Eye Institute, Baltimore, MD
Funded by Dr. James and Elizabeth Wise
Project: Neuroprotection through Altered Scleral Biomechanics

Download Dr. Pitha's final project research poster (PDF) »

Final Report Summary: To date, the only way to stop vision loss from glaucoma is intraocular pressure (IOP) reduction by daily medication use, laser procedure, or incisional surgery. In some patients IOP reduction is difficult to accomplish or glaucomatous vision loss occurs despite substantial IOP reduction.

These clinical situations highlight the need for development of IOP-independent, glaucoma treatment strategies otherwise known as neuroprotection. One promising neuroprotective therapeutic for glaucoma treatment is the blood pressure medication losartan. Losartan’s protective activity is due to prevention of remodeling processes that occur in the wall of the eye (the sclera) during glaucoma.

In these studies we have shown that losartan treatment targets specific cells within the sclera called fibroblasts. Fibroblasts exposed to losartan are prevented from becoming “activated” and remodeling the scleral tissue. In addition, we have developed long-lasting, drug releasing microparticles to prevent scleral remodeling in glaucoma.


Carla J. Siegfried, MD
Washington University School of Medicine, St. Louis, MO
Funded by The Alcon Foundation
Project: Pathological Alterations in the Trabecular Meshwork Following Vitrectomy and Lens Extraction: A Model of Oxidative Stress

Download Dr. Siegfried's final project research poster (PDF) »

Final Report Summary: Elevation of pressure in the eye is the only risk factor for glaucoma that can be modified. Improved understanding of how the eye’s natural drain is damaged can provide insights to new treatments and prevention of this blinding condition.

We have measured oxygen levels inside the eyes of patients undergoing eye surgery with a small probe and found increased oxygen levels in patients who have had removal of the gel in the back of the eye, a procedure performed for various retinal diseases. Patients who have had this procedure nearly always require cataract surgery and this combination of procedures lead to an increased risk of glaucoma. This excess oxygen may be the source of molecules that cause damage to the cells of the natural drain of the eye. In addition, the level of antioxidants, compounds that protect the cells from this damage, are decreased following this combination of surgeries.

By performing these two procedures (removal of gel and then lens removal), we predicted increased oxygen levels in the front of the eye in the area of the natural drain in a glaucoma model. We were unable to duplicate these findings in this model, but did enhance our techniques utilizing a laser to dissect these specific cells in the drain of the eye to study changes associated with damage and then study the how these cells may have altered programming of their genetic code. In this manner, we can now learn more precisely how these cells are damaged and potentially identify patients who are at risk for damage and new ways to treat glaucoma.


For her research project exploring the role of oxygen and antioxidant levels in the eye, Dr. Siegfried was awarded the 2018 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.


W. Daniel Stamer, PhD
Duke University Eye Center, Durham, NC
Funded by The Alcon Foundation
Project: Role of Exosomes in Glaucomatous Lamina Cribrosa Remodeling

Final Report Summary: In this project we have optimized techniques to isolate and characterize exosomes from lamina cribrosa cells. Exosomes are small vesicles that are released by cells to perform a variety of functions. In the lamina cribrosa, like the trabecular meshwork we hypothesize that exosomes participate in the turnover of extracellular matrix and homeostatic signaling with cell neighbors, particularly in response to elevations in intraocular pressure/pulsations. In the present study we mimicked pressure pulsations by cyclically stretching lamina cribrosa cells and collecting/purifying released exosomes from the cell culture media. We observed that exosomes from glaucomatous lamina cribrosa cells were different than exosomes from normal cells. These differences hold the potential to provide information about abnormal remodeling of the optic nerve head in early stages of glaucoma.


Evan B. Stubbs, Jr., PhD
Edward Hines, Jr. VA Hospital, Hines, IL
Funded by The Alcon Foundation
Project: Mitochondrial-specific Antioxidant XJB-3-151 as a Novel Therapeutic Strategy to Lower Elevated Intraocular Pressure

Download Dr. Stubbs' final project research poster [1 of 2] (PDF) »

Download Dr. Stubbs' final project research poster [2 of 2] (PDF) »

Final Report Summary: Glaucoma is a silent disease that, over time, kills the nerve cells of the retina leading to irreversible blindness. Current treatment options are restricted to non-specific interventions aimed at lowering intraocular pressure (IOP). For many glaucomatous patients, however, pharmacological and surgical management of IOP does not always help. The development of targeted therapeutic strategies directed at the cause of elevated IOP is critical for the advanced management of glaucoma. The cause of elevated IOP most likely involves a molecule called transforming growth factor-β2 (TGF-β2). Funding support from the Glaucoma Research Foundation Shaffer Grant has allowed our lab to advance our understanding of exactly how TGF-β2, a multifunctional cytokine, promotes increases in IOP of patients with POAG. We found that specific cells in the eye, called TM cells, constitutively express and secrete TGF-β2, highlighting the TM as a viable targetable source of TGF-β2. This molecule was further found to elicit harmful and pronounced oxidative stress to the TM. Our findings are consistent with other studies also reporting elevated levels of oxidative stress markers in the eyes of POAG patients, along with altered expression of antioxidant defenses in the TM. Results from this Shaffer Grant study also show that targeting antioxidants such as XJB-5-131 to the TM significantly attenuates expression and release of TGF-β2 from cultured human TM cells. Of equal importance, XJB-5-131 protected human primary TM cells against TGF-β2 mediated changes in expression of specific extracellular matrix proteins. These exciting findings are being put to the challenge to see if targeting antioxidants to the TM in porcine and human eyes will lower IOP. To do this, we have encapsulated small beads, called nanoparticles, with various test agents. We are seeing, for the first time, that these nanoparticles can markedly reduce IOP by reducing endogenous expression of TGF-β2. Collectively, our findings support targeted disruption of constitutive TGF-β2 expression within the eye using antioxidant-encapsulating nanoparticles and raises enthusiasm that this strategy will be a clinically useful and effective new therapy by which to better manage IOP in patients with POAG.


David A. Sullivan, MS, PhD, FARVO
Co-investigator: Louis R. Pasquale, MD
Schepens Eye Research Institute, Massachusetts Eye and Ear, Harvard Medical School, Boston, MA
Dr. Henry A. Sutro Family Grant for Research
Project: Estrogen & Glaucoma

Download Dr. Sullivan's final project research poster (PDF) »

Final Report Summary: Glaucoma is characterized by a gradual loss of retinal ganglion cells (RGCs), which leads to a loss of vision. The most common form of glaucoma, occurring in 70 to 90% of patients, is primary open angle glaucoma (POAG).

One of the most compelling epidemiological features of POAG is that its incidence shows a striking sex-related difference. Women have a significantly lower incidence of POAG, as compared to men, until the age of 80 years. This sex-related difference has been linked to the extent of lifetime estrogen exposure. Indeed, there is a strong assocation between increased estrogen exposure and a reduced POAG risk. Conversely, studies have shown that a decreased exposure (i.e. early loss of estrogens), confers an increased risk of POAG. We hypothesize that an early estrogen deficiency accelerates the aging of the optic nerve and predisposes this nerve to glaucomatous damage.

To test our hypothesis we determined whether early estrogen deficiency is associated with heightened intraocular pressure, RGC loss and glaucoma in an animal model. Our results demonstrate that estrogen deprivation does promote the development of glaucoma in female mice. To continue these studies, we seek to determine whether estrogen administration will serve as a novel preventive treatment for glaucoma, and in particular, POAG. If so, our research will have significantly advanced our understanding of the role of estrogen in the pathophysiology of glaucoma.

The 2015 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Paul L. Kaufman, MD
University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin
Co-funded by The Alcon Foundation
Project: Gene Therapy for Glaucoma

Matthew A. Smith, PhD
University of Pittsburgh, Pittsburgh, PA
Project: Measuring the In-vivo Effects on the Optic Nerve Head of Acute Variations in Cerebrospinal Fluid Pressure


Gülgün Tezel, MD
Columbia University, New York, NY
Project: Molecular Biomarkers of Glaucoma

In September 2015, IOVS (vol. 56 no. 10) published results from this research project in "Proteomics Analysis of Molecular Risk Factors in the Ocular Hypertensive Human Retina." The published paper concluded that" "molecular alterations detected in the ocular hypertensive human retina as opposed to previously detected alterations in human donor retinas with clinically manifest glaucoma suggest that proteome alterations determine the individual threshold to tolerate the ocular hypertension-induced tissue stress or convert to glaucomatous neurodegeneration when intrinsic adaptive/protective responses are overwhelmed."

The 2015 Shaffer Grants for Innovative Glaucoma Research

Donald L. Budenz, MD, MPH
University of North Carolina, Chapel Hill, NC
Dr. Henry A. Sutro Family Grant for Research
Project: Incidence of Glaucoma and Glaucoma Progression in an Urban West African Population


Richard T. Libby, PhD
University of Rochester Medical School, Rochester, NY
Funded by The Alcon Foundation

Project: Understanding Axonal Degeneration Pathways in Glaucoma


For his research project to explore a novel idea in the field of neurodegeneration, defining the molecular cascade that controls axon degeneration, which is a key early event in glaucoma, Dr. Richard Libby was awarded the 2017 Shaffer Prize from Glaucoma Research Foundation. The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

Paloma Liton, PhD
Duke University Eye Center, Durham, NC
Funded by Dr. James and Elizabeth Wise
Project: Lysosomal Enzymes, Glycosaminoglycans and Outflow Pathway Physiology

Lyne Racette, PhD
Indiana University, Indianapolis, IN
The Dr. Miriam Yelsky Memorial Research Grant
Project: Early Detection of Glaucoma Progression using Structural and Functional Data Jointly

Shandiz Tehrani, MD, PhD
Oregon Health & Science University, Portland, OR
Funded by The Alcon Foundation
Project: Local Drug Delivery to the Optic Nerve Head as a Novel Treatment in Experimental Glaucoma

The 2014 Shaffer Grants for Innovative Glaucoma Research

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

Vikas Gulati, MD
Truhlsen Eye Institute, University of Nebraska Medical Center, Omaha, Nebraska
Funding provided by a grant from The Alcon Foundation
Project: Effect of Vascular Endothelial Growth Factor Blockers on Aqueous Humor Dynamics

David Krizaj, PhD
Moran Eye Institute, University of Utah, Salt lake City, Utah
Funding provided by Dr. James and Elizabeth Wise
Project: RGC Mechanotransduction as a Target in Glaucoma


Dr. Liu in the lab

Yutao Liu, MD, PhD
Medical College of Georgia, Georgia Regents University, Augusta, Georgia
Funding provided by a grant from The Alcon Foundation

Project: Exosomal RNAs and Aqueous Humor Dynamics

Dr. Liu's research results from this study were published in the January 18, 2015 edition of the peer-reviewed journal Experimental Eye Research, and the February 1, 2018 issue of the journal Human Molecular Genetics.


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


For his research project to determine whether therapies can be designed to modulate the immune system to prevent vision loss and blindness in glaucoma patients, Stuart J. McKinnon, MD, PhD was awarded the 2016 Shaffer Prize for Innovative Glaucoma Research.

The Shaffer Prize, presented annually by Glaucoma Research Foundation, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

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

Colm O’Brien, MD, FRCS
Mater Misericordiae University Hospital, Dublin, Ireland
Funding provided by a grant from The Alcon Foundation
Project: Caveolins, Calcium Signalling and Fibrosis of Lamina Cribrosa Cells in Glaucoma

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

2013 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


John H. Fingert, MD, PhD
University of Iowa, Department of Ophthalmology and Visual Sciences, Iowa City, Iowa

Project: Molecular Genetic Study of Normal Tension Glaucoma using Transgenic Mice

In February 2015, Ophthalmology Times reported that Dr. Fingert's continuing research provides strong evidence that mutation of the TBK1 gene can lead to glaucoma and may provide insights into disease mechanisms and future treatments. “Hopefully this will open up a new field for low-pressure glaucoma research and treatment,” Dr. Fingert said. He presented his research results at the 2014 meeting of American Academy of Ophthalmology.


Yvonne Ou, MD
University of California San Francisco, Department of Ophthalmology, San Francisco, California

Project: Investigating Axonal Death Pathways in Glaucoma

"Our goal was to investigate the parts of the optic nerve cell, specifically axons and synapses, which may be vulnerable early in the course of the disease."

David Sretavan, MD, PhD
University of California San Francisco, San Francisco, California

Project: Pathophysiological Progression in Single RGC Axons Following Microscale Compressive Injury

2013 Shaffer Grants for Innovative Glaucoma Research

Anneke I. den Hollander, PhD
Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands
The 2013 Dr. Miriam Yelsky Memorial Research Grant

Project: Dissecting the Genetic Causes of Congenital and Juvenile Glaucoma


M. Elizabeth Fini, PhD
University of Southern California, Institute for Genetic Medicine, Los Angeles, California
Funding provided by a grant from the Merck Department of Continuing Education

Project: Novel Mucins and Aqueous Outflow

Recent studies suggest that the glycocalyx in the outflow pathways of the eye may be much more extensive than previously imagined. The idea that mucins might be present in this lining layer and play a role in ocular hypertension has not been previously considered. If confirmed, the findings will open a new line of research that could ultimately lead to significant innovation, as drugs that control amounts of the novel mucins or that target specific glycosylating enzymes could lead to a new treatment paradigm for glaucoma.


Andras M. Komaromy, DrMedVet, PhD
Michigan State University, East Lansing, Michigan
Funding provided by a grant from The Alcon Foundation

Project: Gene Therapy in a Spontaneous Canine Model of Primary Open-Angle Glaucoma


For his research on the potential of gene therapy to provide lasting control of intraocular pressure in glaucoma patients with known genetic defects, András Komáromy, DVM, PhD was awarded the 2015 Shaffer Prize for Innovative Glaucoma Research. The Shaffer Prize, presented annually by the GRF Scientific Advisory Committee, recognizes a researcher whose project best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma. Dr. Komáromy studies the molecular causes of inherited eye diseases in dogs and is working to develop gene therapies to stop vision loss. By identifying and treating gene mutations in dogs, his research moves us closer to gene therapy that could one day be used to manage and prevent glaucoma in humans.

Colleen M. McDowell, PhD
University of North Texas Health Science Center, Fort Worth, Texas
Funding provided by a grant from The Alcon Foundation

Project: Retina Ganglion Cell Subtype Specific Cell Death in a Mouse Model of Human Primary Open-Angle Glaucoma

Lin Wang, MD, PhD
Devers Eye Institute/Legacy Research Institute, Portland, Oregon
Funding provided by a grant from The Alcon Foundation

Project: Noninvasive Assessment of Dynamic Autoregulation in Optic Nerve Head

2012 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Leonard A. Levin, MD, PhD, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin

Project: Sustained-Release Formulations of Redox-Active Drugs for Neuroprotection in Glaucoma


Alexander C. Theos, PhD, Georgetown University, Washington, D.C.

Project: GPNMB Deficiency and Associated Cytotoxicity in Pigment Dispersion Syndrome, a Precursor of Pigmentary Glaucoma

Dr. Theos' research results were published in an article titled "PKD Domains Distinguish PMEL and GPNMB Localization" in a 2013 edition of the peer-reviewed journal Pigment Cell & Melanoma Research. "This work would not have been completed without the support of the Glaucoma Research Foundation," Dr. Theos said.


Derek S. Welsbie, MD, PhD, The Johns Hopkins University School of Medicine, Baltimore, Maryland

Project: Evaluating the Role of the c-Jun N-terminal Kinase Cascade in Retinal Ganglion Cell Death

Dr. Welsbie's research results were published in an article titled "Functional genomic screening identifies dual leucine zipper kinase as a key mediator of retinal ganglion cell death" in the March 5, 2013 edition of the peer-reviewed journal PNAS (Proceedings of the National Academy of Sciences).


Dr. Welsbie was awarded the 2014 Shaffer Prize for Innovative Glaucoma Research by the Glaucoma Research Foundation. The Shaffer Prize recognizes the researcher whose project, funded by a Shaffer Grant in a given year, best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.

2012 Shaffer Grants for Innovative Glaucoma Research

David Andrew Feldheim, PhD, University of California Santa Cruz, Santa Cruz, California

Project: Transcriptional Control of RGC Health and Function

Purushottam Jha, PhD, University of Arkansas for Medical Sciences, Little Rock, Arkansas

Project: Complement System as Therapeutic Target for Glaucoma


Melanie Kelly, PhD, Dalhousie University, Halifax, Nova Scotia, Canada

Project: Manipulating Lipid Signaling to Treat Glaucoma and Ocular Disease

Dr. Kelly reports: "Our research was able to accomplish all of the aims for this project." Her laboratory's findings were published in the April 11, 2103 issue of the journal Neuropharmacology (Slusar et al., 2013)

Wei Li, PhD, University of Miami School of Medicine, Miami, Florida

Project: Global Mapping of Glaucoma Autoantibody Biomarkers

Rachel Wong, PhD, University of Washington, Seattle, Washington

Project: Exploring Loss and Recovery of Visual Receptive Field Properties in Populations of Retinal Ganglion Cells in a Glaucoma Model

2011 Frank Stein and Paul S. May Grants for Innovative Glaucoma Research


William H. Baldridge, PhD, Dalhousie University, Halifax, NS Canada

Project: Calcium-permeable AMPA Receptors and Retinal Ganglion Cell Death during Glaucoma

"This study investigated the D-serine modulation of non-NMDA ionotropic glutamate receptors expressed by inner retinal neurons. To our knowledge, this is the first study to address specifically the effect of D-serine on AMPA ⁄ kainate receptors in intact central nervous system tissue, to identify its effect on calcium permeable AMPA receptors and to report the endogenous inhibition of AMPA ⁄ kainate receptors." - from the abstract of Dr. Baldridge's paper published in volume 35 of the European Journal of Neuroscience, 2012.

Hani Levkovitch-Verbin, MD, MPA, Goldschleger Eye Institute, Tel Hashomer, Israel

Project: Age-related Increased Vulnerability of Retinal Ganglion Cells to Elevated IOP- Mechanism and Neuroprotection.

Keith R. Martin, PhD, Cambridge Centre for Brain Repair, Cambridge, United Kingdom

Project: Pre-clinical Assessment of Human Retinal Ganglion Cell Neuroprotection by Human Stem Cells: Efficacy and Mechanism.

2011 Shaffer Grants for Innovative Glaucoma Research

Eduardo J. Chichilnisky, PhD, The Salk Institute, La Jolla, CA

Project: Physiological Changes and Loss of Distinct Ganglion Cell Types in Glaucoma


Gareth R. Howell, PhD, The Jackson Laboratory, Bar Harbor, ME

Project: Understanding the Mechanisms of Wlds-mediated Protection in Glaucoma


Dr. Gareth Howell was awarded the 2013 Shaffer Prize for Innovative Glaucoma Research for his study investigating the mechanism by which a spontaneous mutation (Wallerian degeneration slow, Wlds) prevents retinal ganglion cell death in glaucoma. The Shaffer Prize recognizes the researcher whose project, funded by a Shaffer Grant in a given year, best exemplifies the pursuit of innovative ideas in the quest to better understand glaucoma.


Janice Vranka, PhD, Oregon Health & Science University, Portland, Oregon

Project: Versican as Primary Contributor to Aqueous Humor Outflow Resistance

Dr. Vranka’s project studied Versican, a large proteoglycan that is known to interact with many other proteins also present in the trabecular meshwork, which is thought to be the primary contributor to outflow resistance. Understanding of the overall structure and organization of the outflow resistance, which directly affects the intraocular pressure system will help to enable the development of better treatments to reduce pressure for primary open-angle glaucoma patients. Dr. Vranka’s findings were published in the July 2011 issue of Investigative Ophthalmology & Visual Science (IOVS).

Shunbin Xu, MD, PhD, Rush University Medical Center, Chicago, Illinois

Project: MicroRNAs in Retinal Ganglion Cells and Glaucomatous Neurodegeneration.

2010 Shaffer Grants

Emmanuel Buys, PhD, Massachusetts General Hospital, Boston, Mass.

Project: Soluble guanylate cyclase alpha 1-deficient mice: a novel murine model of elevated IOP and glaucoma


Tonia S. Rex, PhD, University of Tennessee Health Science Center, Memphis, Tenn.

Project: Systemic Delivery of a Neuroprotective Agent to Protect against Glaucomatous Cell Death in the DBA2/J Mouse


Dr. Rex was awarded the 2012 Shaffer Prize for Innovative Glaucoma Research for her research investigating the effectiveness of a neuroprotective therapy in a model of inherited glaucoma.

Dr. Rex used gene delivery to provide long-term production of a modified form of erythropoietin (EPO), a hormone that induces red blood cell production but is also a neuroprotective cytokine. Gene delivery is ideal for glaucoma since it is a slowly progressing retinal degenerative disease. The Rex lab used the DBA/2J mouse model of pigment dispersion glaucoma. They treated prior to the onset of cell death, then monitored intraocular pressure and counted the number of surviving retinal ganglion cells.


Yi Zhao, PhD, Ohio State University, Columbus, Ohio

Project: Nanoengineered In Vitro Trabecular Meshwork ™ Model for Systematic Investigation of Aqueous Humor Outflow Resistance

This project developed an in vitro model using 3D porous polymer for studying the aqueous humor outflow in the eye. The results show that the in vitro model is a useful alternative to human donors because it allows parallel screening of a wide array of potent parameters that may regulate intraocular pressure. It provides a promising solution for unveiling the underlying mechanism of primary open-angle glaucoma and exploring effective therapeutics. Several proceeding papers and abstracts were published in conferences related to eye research and biomedical micro/nanotechnology, including the journals Biomedical Microdevices and Annals of Biomedical Engineering.


An Zhou, PhD, Robert S. Dow Neurobiology Laboratories, Portland, Oregon

Project: Epigenetic regulation of HIOP-induced endogenous neuroprotection in rat retinas

“In this GRF-supported study, we treated retinas with three related but different, high IOP-induced ischemic conditions: preconditioning (short ischemia, causing litter injury), injurious (prolonged ischemia, severe injury), and tolerant (preconditioning followed by prolonged ischemia, protected from injury). For retinas prepared from these three experimental conditions, we performed proteomic analyses using the latest technology so that proteins that are uniquely regulated under each condition can be identified. We then performed neuroanatomical analyses to validate proteomic findings and analyzed additional proteins that were suggested by proteomic findings. As a result, we report that, in ischemic-injured or ischemic-tolerant retinas, there is a striking difference in the abundance of a number of proteins that we know play important roles in neuroprotection against ischemic injury in brain. These proteins, if their roles in neuroprotection in the retina are fully established in the future by more comprehensive studies, may present novel therapeutic targets in treating retinal disorders including glaucomatous conditions.” Dr. Zhou's findings were published in the International Journal of Physiology, Pathophysiology and Pharmacology.

2009 Shaffer Grants


Haiyan Gong, MD, PhD, Boston University School of Medicine, Boston, Mass.

Project: A Study of the Dynamics of Schlemm's Canal Endothelial Cells using a Three-dimensional Cell Culture Device with Real-time Imaging. (Pictured: Dr. Gong examines samples using an electron Microscope).

"Schlemm's canal endothelial cells are believed to be one of the resistance sites crossed by the aqueous humor before entering the blood circulation and are likely to play an important role in the regulation of aqueous humor outflow resistance. In this study, we modified and applied a three-dimensional (3D) cell culture device which was recently developed at MIT to study the dynamics of Schlemm's canal endothelial cells. Our results demonstrated that our 3D cell culture device enables a real-time imaging of giant vacuole formation and tracers crossing the cultured endothelial cell monolayer in a controlled experimental condition. We showed that using a chemical, which can induce the cell into a more relaxed state, can promote giant vacuole formation. This result translates to an increase in drainage of aqueous humor and a decrease in pressure within the eye, similar to results established in animal models. This finding further validates our 3D cell culture devices as an experimental model for future glaucoma studies."


Deborah C. Otteson, PhD, University of Houston College of Optometry, Houston, Texas

Project: The Role of DNA Methylation in Regulating Eph Receptor Expression in the Retina

Dr. Otteson studied how retinal ganglion cells turn on and off the genes that regulate the normal patterns of connections during optic nerve development. Her overall aim was to enhance the development of regenerative therapies to restore the optic nerve and vision in glaucoma patients. She published the results of her findings in the September, 2010 edition of the journal Vision Research.

2008 Shaffer Grants

Paul Habib Artes, PhD, Dalhousie University, Halifax, NS, Canada

Project: Analysis of Progression in Glaucoma

Jamie Craig, PhD, Flinders University of South Australia

Project: Genome-wide Association in Primary Open Angle Glaucoma: The Blindness in Glaucoma Genetic Epidemiology Relative Risk Study

Brad Fortune, OD, PhD, Devers Eye Institute, Portland, Oregon

Project: Imaging the Course of Axonal Degeneration in Experimental Glaucoma


Kate E. Keller, PhD, Casey Eye Institute, Portland, Oregon

Project: RNAi Gene Silencing of Enzymes in the Glycosaminoglycan Biosynthetic Pathway


Dr. Keller was awarded the 2010 Shaffer Prize for Innovative Glaucoma Research for her research investigating the role of Glycosaminoglycans (GAGs) in fluid outflow resistance in the trabecular meshwork of the eye. Experimental results from this study could potentially lead to new therapies for lowering eye pressure in patients with primary open-angle glaucoma. Dr. Keller published her results in the scientific journals Investigative Ophthalmology and Visual Science and Experimental Eye Research.

Raquel L. Lieberman, PhD, Georgia Institute of Technology, Atlanta, Georgia

Project: Development of Pharmacological Chaperone Therapy for Inherited Primary and Juvenile Open Angle Glaucoma


Yutao Liu, MD, PhD, Duke University Medical Center, Durham, North Carolina

Project: Investigation of Gene Copy Number Variants in Primary Open Angle Glaucoma

"Thanks very much for your support of my research project in 2008. Your funding support initiated my CNV research program in POAG. With your funding, I then obtained further research funding from Duke Translational Research Institute in 2009 and American Health Assistance Foundation in 2010. Now I have published my research in PLoS ONE journal. Our work is the first to establish the potential connection between Krabbe disease and POAG. We found that GALC deletion could contribute approximately 1% of POAG cases. The GALC deletion carrier has 3-5 times more risk than a non-carrier."

For information about grants awarded prior to 2008, please contact the Glaucoma Research Foundation at (415) 986-3162 or research@glaucoma.org.

Last reviewed on February 24, 2021

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