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National Glaucoma Research - Current Awards

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. 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. Yiqin Du

Yiqin Du, MD, PhD

Pittsburgh, PA
University of Pittsburgh

Title: A Mouse Glaucoma Model and Cell Therapy for Glaucoma
Non-Technical Title: Cell Therapy in A Mouse Model with Increased Eye Pressure
Duration: July 1, 2014 - June 30, 2016

Summary: Glaucoma is a leading cause of irreversible blindness. Elevated intraocular pressure (IOP) is a major risk factor for glaucoma, and it is controllable. The trabecular meshwork (TM), spongy issue near the surface of the eyeball, acts as a drainage system for the aqueous humor, a transparent, gelatinous fluid that fills the space between the lens and the cornea of the eye and nourishes the lens. When this TM drainage system becomes blocked, as can happen from irregularities in the cells and matrix of the meshwork, the blockage can lead to a build-up of aqueous fluid in the eye and subsequent elevation of IOP. We have isolated and characterized immature cells from the TM with the ability to seek out and repair the damage in this tissue. Our research will consist of modelling elevated pressure by damaging the TM in a mouse model and then attempting to rebuild and restore a functioning meshwork and reduce the intraocular pressure with cell therapy using immature TM cells.
More details

Program: Glaucoma
Award Type: Standard
$100,000

Acknowledgements: This grant is made possible in part by a bequest from the estate of June Mae Metzger.



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. Baojian Fan

Baojian Fan, MD, PhD

Massachusetts Eye and Ear Infirmary
Boston, MA

Title: Discovery of Pigment Dispersion Syndrome and Pigmentary Glaucoma Genes by Exome Sequencing
Non-Technical Title: Finding Genes that Cause Pigment Dispersion Syndrome and Pigmentary Glaucoma
Duration: July 1, 2014 - June 30, 2016

Co-PI(s):
Janey L. Wiggs, MD, PhD
Massachusetts Eye and Ear Infirmary

Summary: Pigment dispersion syndrome (PDS) causes pigmentary glaucoma, which is a common form of open-angle glaucoma that usually affects young adults and can be inherited. No genes responsible for this condition have been identified yet in humans. In our proposed research, we will use whole exome sequencing, a new and powerful technology, to find genes that can cause this common form of glaucoma. The results from this project can be used to develop new methods of diagnosis and treatment for PDS and pigmentary glaucoma.
More details

Program: Glaucoma
Award Type: Standard
$100,000



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. Jeff Gidday

Jeff Gidday, PhD

Washington University School of Medicine
St. Louis, MO

Title: Hypoxic Conditioning for Protection in DBA/2J Glaucoma Model
Non-Technical Title: Glaucoma Protection by Repeated Adaptive Stress
Duration: July 1, 2014 - June 30, 2016

Summary: A fundamental principle of biology and evolution is that organisms, and cells, adapt to a stress imposed on them so that they can better handle that stress if they encountered it again in the future. The studies in this research project are designed to leverage this concept as a way of protecting the eye from glaucoma. In particular, we will test whether intermittently exposing mice to a hypoxic (ie, low-oxygen) stress, that by itself is not harmful, will trigger adaptive responses in the eye that make it more resistant to the damaging effects of glaucoma. If successful, these studies will confirm the presence of innate protective responses in the eye that someday could be activated in humans with glaucoma, thereby reducing the vision loss and blindness that characterize this devastating disease.
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 - December 31, 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