Glaucoma Research Foundation

Pilot Project Grants Awarded

Each year the Glaucoma Research Foundation awards pilot project research grants to worthy investigators with innovative ideas. Following are summaries of grants awarded annually from 2006 through 2008 at $40,000 each.

For information about prior years’ Pilot Project grants or to request a copy of a research project’s final report, please send an email to research@glaucoma.org.

See this year’s grant recipients in the Shaffer Fund for Innovative Glaucoma Research.

2008 Shaffer Grants Awarded

Paul Habib Artes, PhDr
Dalhousie University, Halifax, NS, Canada
Analysis of Progression in Glaucoma
When patients with glaucoma are followed over time, the aim is to detect worsening of the disease and to measure its rate, so that the therapy can be optimally tailored to the individual patient’s risk of sight loss. The idea of this project is to take a patient’s measurements from several visits, randomly re-arrange them, and compare the real data with the randomly re-arranged data. This is done many hundreds or thousands of times until a complete distribution of the possible random change estimates emerges. The aim is to translate these findings into terms that clinicians and patients can readily understand.

Jamie Craig, PhD
Flinders University of South Australia
Genome-wide Association in Primary Open Angle Glaucoma: The Blindness in Glaucoma Genetic Epidemiology Relative Risk Study
Finding common genetic markers which lead to glaucoma blindness. Dr. Craig’s lab used well-characterized cohorts of severe cases of glaucoma, and the power of high density gene screening to identify multiple genetic risk factors leading to poor outcomes in glaucoma.

Brad Fortune, OD, PhD
Devers Eye Institute, Portland, OR
Imaging the Course of Axonal Degeneration in Experimental Glaucoma
Retinal nerve fiber layer (RNFL) defects may be one of the earliest signs of damage in glaucoma. The majority of eyes with elevated intraocular pressure already have clinically detectable RNFL defects before reproducible abnormalities first appear in the visual field. Dr. Fortune’s lab tested the hypothesis that degradation of axonal NF and/or MT is clinically detectable and precedes complete degeneration and loss of RGC axons in an experimental model of glaucoma.

Kate E. Keller, PhD
Casey Eye Institute, Portland, OR
RNAi Gene Silencing of Enzymes in the Glycosaminoglycan Biosynthetic Pathway
In primary open-angle glaucoma (POAG), there is increased resistance to aqueous flow through the trabecular meshwork TM, which results in increased intraocular pressure (IOP). Glycosaminoglycans (GAGs) are a likely source of outflow resistance. Results from the experiments proposed here investigated the role of GAG chains in outflow resistance and may lead to new therapies for POAG patients.

Raquel L. Lieberman, PhD
Georgia Institute of Technology, Atlanta, GA
Development of Pharmacological Chaperone Therapy for Inherited Primary and Juvenile Open Angle Glaucoma
Dr. Lieberman’s lab aims to develop a new therapy for inherited glaucoma, many cases of which are caused by mutations in a protein called myocilin. Myocilin forms part of the trabecular extracellular matrix, or TEM, which is important in regulating eye pressure. When the matrix doesn’t function correctly, eye pressure increases, leading to retinal degeneration and vision loss.

Yutao Liu, MD, PhD
Duke University Medical Center, Durham, NC
Investigation of Gene Copy Number Variants in Primary Open Angle Glaucoma
Dr. Liu’s lab investigated DNA copy number variants (CNVs), a form of genetic variation associated with inherited diseases, in patients with primary open-angle glaucoma (POAG). This study may lead to the identification of novel genetic components that increase individual risk to POAG and will improve our understanding of the inherited mechanisms of POAG.

2007 Pilot Project Grants Awarded

Ruth Ashery-Padan, PhD
Tel Aviv University, Israel
Discovering the Roles tf Pax6 in the Development of the Trabecular Meshwork and Schlemm’s Canal
Dr. Ashery-Padan’s analysis should provide an important step for the development of therapeutic strategies to treat patients with congenital and juvenile glaucoma.

Donald J. Brown, PhD
University of California, Irvine
Pressure Induced Dynamic 3D Changes in Lamina Cribrosa using Second Harmonic Imaging Microscopy
The data from this study should provide critically important insights as to how eye pressure causes vision damage.

Christopher A. Girkin, MD MSPH
University of Alabama, Birmingham, AL
Development of a Model for the Study of the Role of the Lamina Cribrosa in Development and Progression of Glaucoma
The development of a glaucoma model in the tree shrew will provide a resource to study the connective tissue changes within the lamina cribrosa and neurodegenerative changes in the retina, optic nerve, and brain.

Sharon A. Haymes, PhD
Dalhousie University, Halifax, Nova Scotia, Canada
Strategies Used by Glaucoma Patients to View Real-World Scenes
Falls and motor vehicle collisions are leading causes of injury in people with glaucoma. This study may result in the development of prevention programs, patient education, and the enhancement of quality of life for people with glaucoma.

Brian A. Link, PhD
Medical College of Wisconsin, Milwaukee, WI
Using Zebrafish to Identify Genes that Promote Retinal Ganglion Cell Degeneration in the Context of Elevated Intraocular Pressure
Once the key genes for glaucoma are identified, genetic tests can be developed and ultimately, research for targeted therapies can begin.

2006 Pilot Project Grants Awarded

Jonathan G. Crowston MD, PhD
Hamilton Glaucoma Center, University of California, San Diego
The Neuroprotective Effect of Diet Restriction on Retinal Ganglion Cell Death
Dr. Crowston’s lab developed sensitive methods for quantifying retinal ganglion cells in living, genetically modified mice, which have florescent retinal ganglion cells. They used in-vivo imaging to examine the neuroprotection afforded by dietary restriction. Dietary restriction has been shown to delay aging and prevent neuron dysfunction and degeneration in a number of experimental models of neurodegeneration including Alzheimers and Parkinson’s disease. These imaging techniques will improve our ability to assess therapies that may prevent retinal ganglion cell loss.

Mark S. Filla, PhD
University of Wisconsin, Madison
Understanding Steroid Induced Changes in IOP: Role of the Cytoskeleton
Dr. Filla’s lab examined the ability of specific cell surface receptors to cause rearrangements in the intracellular skeletal system (the cytoskeleton) in cells that regulate aqueous humor outflow from the eye. This project could lead to a new class of glaucoma therapeutics that are less likely to elicit ocular or systemic side effects as they could specifically target the trabecular meshwork cells that regulate aqueous humor outflow. Watch a video of Dr. Filla discussing his research project.

Thomas Reh, PhD
University of Washington, Seattle
Replacement of Ganglion Cells Through Regeneration
Dr Reh’s lab sought to discover the molecular and cellular road-blocks that limit regeneration in mammals and to determine the feasibility of stimulating the very minimal repair that exists in the mammalian retina to produce new retinal ganglion cells. These experiments could serve as a foundation for developing new therapies for the treatment of glaucoma.

Mark Samuels, PhD
Dalhousie University, Halifax, Nova Scotia, Canada
Genetic Analysis of Nanophthalmos
The study of nanophthalmos and the identification of genes causing this condition should be extremely helpful in understanding the mechanisms underlying more common forms of glaucoma, and may eventually lead to the development of new treatments for glaucoma.

Lin Wang, MD, PhD
Devers Eye Institute/ Discoveries in Sight, Portland, Oregon
Ocular Blood Flow in a Model of Chronically Increased Intraocular Pressure
This study sought to define the relationship between IOP and ocular blood flow and provide insights into the mechanisms by which IOP induces injury in glaucoma. In addition, these data will help clarify apparent discrepancies between previous studies concerning the level of chronic IOP elevation and degree of structural/functional damage observed in these models.