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2012 Research Grants

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

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

We consider it vital to invest funds in new high-impact research that may lead to major government and philanthropic support. Following is a summary of projects we are currently funding (grants made possible by generous support from Alcon, Merck, Frank Stein and Paul S. May, and James Wise, MD).

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

All grants are in the amount of $40,000.


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

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

The goal of Dr. Levin’s project is to explore new ways of preventing retinal ganglion cells (RGCs) and their fibers from dying after they are damaged. Dr. Levin’s lab is investigating a new class of drugs that are highly effective at keeping RGCs alive when the optic nerve is damaged by glaucoma. The problem is that the drugs do not last long enough in the eye, making it impractical for use in patients. In this project they will investigate using tiny nanospheres to deliver their novel drugs and release them slowly over time, which hopefully will preserve vision by maintaining the health of RGCs and the optic nerve.


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 seeks to better understand changes within the cells of the eye that die as a prelude to the development of a type of inherited glaucoma known as pigmentary glaucoma. More specifically, they are looking at the cells that produce the pigment that gives the iris its color. Scientists currently know very little about why these particular cells within the eye do not survive with age and cause problems that lead to a disease called Pigment Dispersion Syndrome (PDS). A specific protein, called GPNMB, is important for keeping cells healthy and is involved in generating and storing pigments. By directly comparing cells that either have normal GPNMB and those that are missing this critical protein, they expect to be able to follow the biology of these cells and better understand why these cells deteriorate in PDS. This will help to eventually develop therapeutics to correct the problem and perhaps prevent these debilitating diseases.


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

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

Glaucoma results from the death of retinal ganglion cells, specialized cells that transmit vision from the eye to the brain. In their absence, the eye continues to sense light but cannot send that signal to the brain. Current therapies all treat the same risk factor, intraocular pressure. Unfortunately, current therapies can produce undesirable side effects, and in some cases, may not halt the disease. Thus, there is a need for new types of drugs that keep the cells alive despite elevated eye pressure (so-called “neuroprotectives”). In glaucoma, normal proteins (cellular machines) are corrupted and cause the retinal ganglion cells to die. One way neuroprotective drugs would work is by interfering with those proteins. Dr. Welsbie’s lab has screened through thousands of proteins and drugs and identified a set of proteins that seem to play a central role in retinal ganglion cell death. They are now trying to better understand these proteins and determine if drugs that target these proteins would treat glaucoma.

The 2012 Shaffer Grants

All grants are in the amount of $40,000.


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

Project: Transcriptional Control of RGC Health and Function

Dr. Feldheim’s project will study transcription factors (TFs) necessary for retinal ganglion cell (RGC) development. The Feldheim lab will focus on testing the role of a TF that is important for the development of RGCs in adult RGC function using genetic techniques. They seek to understand the roles of the transcriptional regulators in adult RGCs, which will provide an important foray into understanding the mechanisms of how RGC health and function are maintained during aging, and how RGC loss is triggered in glaucoma.


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

Project: Complement System as Therapeutic Target for Glaucoma

Glaucoma is one of the leading causes of vision loss. At present, therapies targeting the reduction of intraocular pressure are the only treatment options available to the patients with glaucoma. However, clinical studies have shown that even after lowering the IOP with various drugs does not prevent the progression of vision loss in glaucoma patients. This study by Dr. Jha will lay a foundation for future studies to find the molecular mechanisms involved in the immunopathogenesis of glaucoma (how the immune system’s response figures in the disease). The findings from this study may help in development of specific and effective treatments for glaucoma in future.


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

Project: Manipulating Lipid Signaling to Treat Glaucoma and Ocular Disease

While pressure in the eye (intraocular pressure), is an important risk factor for glaucoma, many other factors are also involved. These may include alterations in blood flow regulation, as well as changes in the ocular immune system. Dr. Kelly’s research project will examine a new class of drugs that may be useful in treating neurodegenerative diseases like glaucoma. These drugs, called endocannabinoid metabolic enzyme inhibitors, can increase the amount of endocannabinoids in the eye. Endocannabinoids are important endogenous signaling molecules in our body and the endocannabinoid system is thought to be one of the body’s natural defense systems against injury. Drugs that increase endocannabinoids may be able to prevent the loss of vision in glaucoma by decreasing the production of harmful chemicals in the retina as well as improving blood flow regulation and preventing inflammation.


Wei Li, PhD, University of Miami School of Medicine, Miami, Fla.

Project: Global Mapping of Glaucoma Autoantibody Biomarkers

A critical barrier to early detection of glaucoma is the lack of biomarkers for reliable diagnosis. Recent studies showed that optic nerve damage in glaucoma triggers the production of autoantibodies, which could be used as biomarkers to glaucoma early detection. Dr. Li’s project will develop a new technology to identify all autoantibodies in the blood and simultaneously quantify their activities like a fingerprint map with thousands of autoantibody peaks at different activities. Statistical comparison will identify all glaucoma-related autoantibodies. A diagnostic model will be developed based on all identified autoantibodies and their activities for more diagnostic accuracy for glaucoma. This new biomarker discovery technology can be applied to different forms of glaucoma in the future to identify autoantibody biomarkers for early detection, diagnosis, subclassification, therapy assessment, and prognosis.


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

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

In this project, Dr. Wong will study the earliest changes in the sensitivity of retinal nerve cells to light, hoping to uncover the first signs and subsequent progression of neuronal dysfunction before cell death. The Wong lab will also determine whether there exists a window in time whereby restoring intraocular pressure to normal levels enables some cells to recapture their original light response properties, or whether once challenged, cells continue to lose visual sensitivity. Together, the knowledge gained in this project will generate new insight into the pathology of the disease as well as help design future therapies for preventing progressive loss of retinal nerve cells and degradation of vision in glaucoma.

Last reviewed on October 29, 2017

This article appeared in the May 2012 issue of Gleams.


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