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National Glaucoma Research - Current Awards

Dr. Michael Girard

Michael Julien Alexandre Girard, Ph.D.

Imperial College London
London, England

Title: In Vivo Corneal Biomechanics: A Biomarker for Glaucoma?
Non-Technical Title: Can Corneal Stiffness Predict Vision Loss from Glaucoma?
Duration: July 1, 2011 - December 31, 2014

Co-PI(s):
Nick Strouthidis, MBBS, M.D., MRCOphth
Moorfields Eye Hospital

Summary: In this project we are exploring the relationship between the mechanical behavior of the cornea, a structure located at the front of the eye, and glaucoma - a potentially blinding condition which affects the optic nerve head, a structure located at the back of the eye. Specifically, we are looking to see whether understanding and quantifying corneal mechanical behavior in humans can be used to predict the likelihood of glaucoma, and of visual loss from glaucoma. This endeavor will have important implications for the diagnosis and management of glaucoma, one of the world's leading causes of blindness.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Curtis  Brandt

Curtis Brandt, Ph.D., FARVO

Board of Regents of the University of Wisconsin System, School of Medicine and Public Health
Madison, WI

Title: Enhancement of Gene Expression for Glaucoma Therapy
Non-Technical Title: An Improved Gene Delivery Method to Lower Eye Pressure in Primate Eyes
Duration: July 1, 2013 - June 30, 2015

Co-PI(s):
Paul Kaufman, M.D.
University of Wisconsin-Madison

Summary: Gene therapy to lower intraocular (eye) pressure is an approach for long-term glaucoma therapy that has the advantage of reducing the number of treatments, thereby improving patient compliance. Drs. Brandt and Kaufman wish to use viral vectors (a disabled virus capable of carrying/transporting genes) to deliver these genes to the front part of the eye where eye pressure is regulated. However, there are factors that limit the ability to produce the desired effect, the reproducibility of the delivery, and, ultimately, the expression of the desired gene. Drs. Brandt and Kaufman will use several approaches to overcome these limitations in order to advance the development of glaucoma gene therapy techniques.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Kevin Chan

Kevin Chan, Ph.D.

University of Pittsburgh
Pittsburgh, PA

Title: Effects of Ocular Hypertension on Visual Brain Damage
Non-Technical Title: Effects of Prolonged Eye Pressure Elevation on Visual Brain Changes
Duration: July 1, 2013 - June 30, 2015

Co-PI(s):
Joel Schuman, M.D.,
University of Pittsburgh
Ian Conner, M.D., Ph.D.
University of Pittsburgh

Summary: Glaucoma is the second leading cause of blindness in the world. Although elevated eye pressure is a major risk factor, recent evidence suggested the involvement of the visual brain, apart from the eye, in the early degenerative mechanisms of glaucoma. Drs. Chan, Conner and Schuman’s goal is to develop new structural, metabolic, and functional magnetic resonance imaging (MRI, a machine that takes detailed images of the inside of the body) techniques for glaucoma. They will make whole-brain, non-invasive and repeated measurements over a period of time to evaluate the damage to the visual pathway and disease progression under different levels of chronic high eye pressure, and monitor for potential neuroprotection after treatment with a drug that lowers eye pressure. The development of novel methods for characterizing chronic glaucoma and neuroprotection in the visual system can potentially lead to more timely intervention and targeted treatments in reducing the burden of this disease.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Peter P. De Deyn

Peter P. De Deyn, M.D., Ph.D.

Institute Born-Bunge
Antwerp, Belgium

Title: Cerebrospinal Fluid Pressure At The Link Between Glaucoma And Alzheimer's Disease
Non-Technical Title: Searching The Link Between Alzheimer's Disease And Increased Risk Of Glaucoma
Duration: July 1, 2012 - June 30, 2014

Co-PI(s):
Debby Van Dam, M.Sc., Ph.D.
Institute Born-Bunge

Summary: Alzheimer's disease patients may be at a high risk of developing glaucoma. Drs. De Deyn, Van Dam, and colleagues are studying the underlying disease mechanisms responsible for this higher risk, both in patients and in mice engineered to have Alzheimer's disease (AD). These investigators hypothesize that reduced pressure in the liquid that surrounds the brain and spine, called cerebrospinal fluid, may be a major factor in this process.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Anna Demetriades

Anna Demetriades, M.D., Ph.D.

Joan and Sanford I. Weill Medical College of Cornell University
New York, NY

Title: Neurotrophic Biofactories for the Treatment of Glaucoma
Non-Technical Title: New Method of Delivering Therapeutic Proteins to the Eye for the Treatment of Glaucoma
Duration: July 1, 2013 - June 30, 2015

Summary: Glaucoma is the result of retinal ganglion cell (RGC) death in the eye which ultimately leads to vision loss in patients. RGCs are the nerve cells that extend down the optic nerve and connect the eye to the brain. The aim of this study is to develop a novel treatment for patients by identifying a new way to slow down and prevent RGC death. Dr. Demetriades’ team will use gene therapy to deliver neuroprotective proteins to specific cells within the retina and determine whether it is best to deliver these proteins directly to RGCs or to adjacent cells in order to optimally improve their survival.
More details

Program: Glaucoma
Award Type: Standard
$100,000

Acknowledgements: This grant is made possible in part by a gift from The New York Community Trust – Steven & Barbara Rothman Fund.



Dr. Chad A. Dickey

Chad A. Dickey, Ph.D.

University of South Florida
Tampa, FL, United States

Title: Disrupting Chaperone/Myocilin Complexes for Glaucoma
Non-Technical Title: Targeting Chaperone Proteins to Improve Glaucoma
Duration: July 1, 2012 - June 30, 2014

Summary: Dr. Dickey and colleagues have determined that a class of proteins termed “chaperones” plays an important part in preserving the proper shape of another protein called myocilin. This is important because mutant myocilin accumulates and kills eye cells important for vision, leading to primary open-angle glaucoma (OAG). The scientists speculate that these chaperones will be excellent drug targets for OAG.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Michael H. Elliott

Michael H. Elliott, Ph.D.

University of Oklahoma Health Sciences Center
Oklahoma City, OK

Title: Caveolins as Novel Mechanosensors in Aqueous Outflow
Non-Technical Title: Novel Mechanism of Control of Aqueous Fluid Drainage
Duration: July 1, 2013 - June 30, 2015

Summary: Elevated eye pressure is a major risk factor for glaucoma and this pressure is regulated by controlling the drainage of fluid from the eye. There are currently no glaucoma medications that target the major pathway of fluid drainage in the eye, yet this pathway is the source of the primary cause and progression in open-angle glaucoma. Dr. Elliott’s project is designed to test a novel mechanism by which the eye regulates fluid drainage and how this mechanism might be dysfunction in glaucoma.
More details

Program: Glaucoma
Award Type: Standard
$100,000

Acknowledgements: Recipient of the Thomas R. Lee Award for National Glaucoma Research



Dr. John H. Fingert

John H. Fingert, M.D., Ph.D.

University of Iowa
Iowa City, IA

Title: Stem Cell Approaches to Glaucoma
Non-Technical Title: Investigating the Biology and Causes of Glaucoma Using Stem Cells
Duration: July 1, 2013 - June 30, 2015

Co-PI(s):
Budd Tucker, Ph.D.
University of Iowa

Summary: Retinal ganglion cells (RGCs) form the optic nerve, which carries vision from the eye to the brain. These ganglion cells are the part of the eye that is primarily affected by glaucoma; however, these cells are very difficult to study in the laboratory. Consequently, the team of Drs. Fingert and Tucker has used a stem cell-based approach to generate RGCs in culture. The team will use these cells to study the mechanism by which a known glaucoma gene, TANK binding kinase 1 (TBK1), leads to RGC loss and eye disease. These studies will provide new insights in the biology of glaucoma and will facilitate the development of new glaucoma therapies.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Philip J Gage

Philip J. Gage, Ph.D.

Regents of the University of Michigan
Ann Arbor, MI

Title: A New, Inducible, and Rapid Model of Glaucoma in Mice
Non-Technical Title: A New, Rapid, and Inducible Model of Glaucoma in Mice
Duration: July 1, 2013 - June 30, 2015

Summary: Mouse models provide an important way to study how mutations in a gene cause disease, and to develop new potential therapies to treat the disease. Dr. Philip Gage’s team has made mice that contain a genetic "switch" that lets them turn off a juvenile glaucoma gene (called Pitx2) in mature mice. These mice appear to provide a model for studying glaucoma that is both inducible and develops rapidly, meaning that they and others should be able to make exciting discoveries more rapidly and at a much cheaper cost. The team plans to look much more carefully at these mice in order to more completely understand how they work.
More details

Program: Glaucoma
Award Type: Standard
$100,000



Dr. Matthew Glucksberg

Matthew Glucksberg, Ph.D.

Northwestern University
Chicago, IL

Title: Effect of Rapid Depressurization on Cultured Cells
Non-Technical Title: Mechanism of Cell Damage in Glaucoma: Effect of Rapid Depressurization on Cells
Duration: July 1, 2013 - June 30, 2014

Co-PI(s):
Mark Johnson, Ph.D.
Northwestern University

Summary: The importance of controlling pressure in the eye is known to be a factor in the damage to vision caused by glaucoma. The reason why controlling pressure is so important is still not known, but there are several hypotheses involving the stresses and strains caused by elevated pressure in the tissue of the optic nerve. However, in recent years a number of studies have supported an alternate hypothesis that it is not the stresses and strains alone that cause the high pressure, but the high pressure itself does the damage. Drs. Gluckberg and Johnson put forward an additional idea that may explain the results of the direct-pressure hypothesis—that is, rapid relief of the applied hydrostatic pressure causes a rapid decompression (related to a process called an “ultra-transient microbubble formation”) that affects cell function.
More details

Program: Glaucoma
Award Type: Standard
$50,000



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Last Review: 08/30/13