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Shaffer Research Grants

When you’re pushing for a breakthrough, novel leads are essential. Shaffer Grants provide seed funds to bold investigators whose creative projects explore promising leads and show strong potential for impact on glaucoma.

shaffer research grants

Glaucoma Research Foundation’s Shaffer Grants program is an innovation incubator, attracting much-needed brainpower to glaucoma research and carrying us closer to a cure. Honoring glaucoma pioneer Robert N. Shaffer, MD, who launched the Foundation, these one-year grants provide $50,000 in seed money for collaborative projects that target one or more of our strategic research goals.

In the spirit of high-risk/high-reward discovery, we consider it vital to invest in new research that may go on to earn major government and additional philanthropic support. The National Institutes of Health and large companies may pass over brilliant young researchers with novel ideas if there is no precedent of support for their work. Armed with evidence made possible by our grants, these scientists often secure the major funding they need to bring their ideas to fruition.

Since 1978, Glaucoma Research Foundation has invested $50 million to advance knowledge through innovative research. Recipients of the first named Shaffer Grants for Innovative Glaucoma Research were announced in 2008 at the Foundation’s 30th Anniversary Benefit. To date, we have awarded more than 275 Shaffer Grants. We will continue to lead the way in research until a cure is found.

2022 Shaffer Research Grants

Kun Che Chang, PhD

Kun-Che Chang, PhD

University of Pittsburgh

Project: A New Therapeutic Gene for RGC Survival and Axon Regeneration in Glaucoma

M. Elizabeth Fini, PhD

M. Elizabeth Fini, PhD

Tufts University

Project: Mechanisms of Steroid-Induced Ocular Hypertension

Sidney Kuo, PhD

Sidney Kuo, PhD

University of Minnesota

Project: Early Structural Changes to Müller Glial Cells in Glaucoma

Myoungsup Sim, PhD

Myoungsup Sim, PhD

Duke University

Project: Primary Cilia-mediated Nitric Oxide Production in Schlemm’s Canal Cells

Brian Soetikno, MD, PhD

Brian Soetikno, MD, PhD

Stanford University

Project: Visible Light OCT for Glaucoma

Qing Wang, MD, PhD

Qing Wang, MD, PhD

Columbia University

Project: Novel Tools to Identify and Target Astrocytic Subtypes to Treat Glaucoma

Past Research Grants

For information about Shaffer Grants and research reports prior to 2012, please contact the Glaucoma Research Foundation.

Kun Che Chang, PhD

Kun-Che Chang, PhD
University of Pittsburgh
Funded by Tania and Michael Stepanian

Project: A New Therapeutic Gene for RGC Survival and Axon Regeneration in Glaucoma

Summary: In patients with glaucoma or other optic neuropathies, damaged retinal ganglion cells (RGCs) die as their axons degenerate. Although many regulators have been reported to function in axon regeneration, regrowth of long-distance axons into the chiasm and brain remains a major challenge. Thus, discovery of new therapeutic factors remains a long-standing research goal. To obtain the synergistic effects of regulators on axon regeneration, we aim to discover new regulators that control different pathways from those already known, which we can then combine for cotreatment therapy. We propose a new pathway involving the molecule identified from prior study. This proposal will assess its role in RGC damage repair using an optic nerve crush model that could translate into therapies for glaucoma and optic neuropathies, which could improve impacted individuals’ quality of life. The results will reveal the functions of this new gene in RGC survival and axon regeneration, which impacts the field by providing a potential therapy for translational studies in patients with glaucoma and optic neuropathies.

M. Elizabeth Fini, PhD

M. Elizabeth Fini, PhD
Tufts University
Funded by the Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Project: Mechanisms of Steroid-Induced Ocular Hypertension

Summary: Ocular hypertension (OH) is the major risk factor for glaucoma, the leading cause of irreversible blindness. Lowering intraocular pressure (IOP) is the only proven treatment. All forms of OH are caused by increased outflow resistance via the conventional outflow pathway comprising the trabecular meshwork (TBM). In open angle OH, pathology is intrinsic to the TBM. This research project focuses on a secondary form of open angle OH caused by treatment with pharmaceutical glucocorticoids (GCs) in the eye. We hypothesize that a protein called ELAVL1is responsible for stabilizing fibronectin mRNA in response to GCs. We will investigate this idea in cultured TBM cells by perturbing ELAVL1 gene expression and assessing the effects on fibronectin stability in the presence and absence of dexamethasone. Study results will be of high impact if our hypothesis is correct, providing the preliminary data for a full study to validate the mechanism in vivo and determine the mechanisms regulating ELAVL1. The ultimate goal is to learn whether GCs directly stimulate expression of a gene, via its GRE, that is responsible for ELAVL1 activation.

Sidney Kuo, PhD

 

Sidney Kuo, PhD
University of Minnesota
Funded by the Frank Stein and Paul S. May Grants for Innovative Glaucoma Research

Project: Early Structural Changes to Müller Glial Cells in Glaucoma

Summary: Higher than normal pressure in the eye (intraocular pressure) is the most common risk factor for glaucoma. Despite intensive research, the mechanisms linking high intraocular pressure and eventual vision loss are not well understood. Based upon preliminary studies in our lab, we hypothesize that pressure-induced changes to the physical structure of Müller glial cells early in disease onset contributes importantly to the eventual death of the retinal ganglion cells, the neurons that transmit visual information from the retina to the brain. To investigate this, we will use high resolution microscopy to image fluorescently-labeled Müller cells and retinal ganglion cells in eyes of mice with experimentally-induced elevated intraocular pressure. By identifying early pathological events in Müller cells, our long-term goal is to provide new insight into possible ways to diagnose and treat glaucoma before retinal ganglion cells are irreversibly lost.

Myoungsup Sim, PhD

 

Myoungsup Sim, PhD
Duke University
Funded by the Dr. Miriam Yelsky Memorial Research Grant

Project: Primary Cilia-mediated Nitric Oxide Production in Schlemm’s Canal Cells

Summary: Elevated intraocular pressure (IOP) results from dysfunction of the conventional outflow pathway, however, the glaucoma drugs targeting this pathway are very limited. Latest studies have shown a potential role of nitric oxide (NO) in lowering IOP. In this context, a NO-donating drug (latanoprostene bunod) was recently approved for the reduction of IOP in patients with ocular hypertension and glaucoma. Nevertheless, most of the NO-based drugs have failed to be approved by FDA due to some challenges related to the exogenous delivery of NO, such as uncontrolled NO release, suggesting that regulation of endogenous NO production could represent a better strategy for glaucoma treatment. NO is produced by the endothelial cells of the Schlemm’s canal (SC), a unique vascular structure component of the outflow pathway. As a result of elevated IOP, SC cells are subjected to fluid flow-induced shear stress, which has been reported to trigger NO production by SC to regulate IOP homeostasis. We seek to investigate how to regulate endogenous NO production in SC cells to improve the NO-based glaucoma therapy. Results of this study will provide an upstream target molecule that can regulate endogenous NO production and advance the current NO-based glaucoma drugs to treat glaucoma patients more safely.

Brian Soetikno, MD, PhD

 

Brian Soetikno, MD, PhD
Stanford University
Funded by Bob and Birdie Feldman & Giving Tuesday contributions

Project: Visible Light OCT for Glaucoma

Summary: Glaucoma is characterized by the damage and death of retinal ganglion cells (RGC) and their retinal nerve fiber layer axons, leading to vision loss. Clinicians rely on diagnostic tests, such as visual field studies and optical coherence tomography (OCT), to diagnose and monitor glaucoma. However, these tests are currently insensitive to detecting glaucoma early and monitoring minute changes in its progression. This proposal will address this need by designing and testing a new OCT imaging device, called visible-light OCT (vis-OCT). Vis-OCT uses visible wavelengths (560 nm +/- 50 nm) to provide ultra-high resolution, three-dimensional imaging (1 to 2 microns) of the retinal layer anatomy. The ultra-high-resolution of vis-OCT enables sub-laminae to be distinguished within the inner plexiform layer (IPL), a site where RGC’s synapse to other retinal neurons. The ability to discern these connections opens the possibility of sensitively detecting RGC damage by measuring the thickness of the sub-laminae. Vis-OCT imaging can be technically challenging due to artifacts from patient eye motion. To solve this issue, we will construct a vis-OCT device with fundus tracking, enabling the acquisition of high-quality images even in the presence of eye motion. Using this novel device, we will image IPL sub-laminae and make measurements of the thicknesses in varying glaucoma stages. This study will provide insight into whether we can detect RGC damage at ultra-high resolution in the IPL. Ultimately, vis-OCT could offer a new imaging biomarker for detecting glaucoma early and monitoring its progression.

Qing Wang, MD, PhD

 

Qing Wang, MD, PhD
Columbia University
Funded by the Dr. Henry A. Sutro Family Grant for Research

Project: Novel Tools to Identify and Target Astrocytic Subtypes to Treat Glaucoma

Summary: Vision loss in glaucoma results from damage to the retinal ganglion cells (RGCs), which are the neurons that connect the eye to the brain. RGC axons from throughout the retina converge at the optic nerve head to exit the eye. A critical insult to RGC axons occurs at the optic nerve head, where they interact extensively with another resident cell type, astrocytes. Astrocytes are thought to play both neuroprotective and neurotoxic roles in complex neurodegenerative diseases, such as glaucoma and Alzheimer’s. Our studies will provide important molecular information and tools for manipulating optic nerve head astrocytes to understand and treat glaucoma. We will use cutting edge single-nuclear RNA sequencing technology to dissect out the molecular pathways that define neurotoxic versus neuroprotective astrocytes in optic nerve heads of glaucoma and normal mouse eyes. We will also develop new viral tools for selectively manipulating genes in optic nerve head astrocytes that can be used for gene therapy approaches by the glaucoma research community. These studies will pave the path for the development of a new avenue of glaucoma therapies directed towards optic nerve head astrocytes.

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