Paul Russell, Ph.D.
The Regents of the University of California-Davis
Davis, CA
Title: Biophysical Cues, Antioxidants and Trabecular Meshwork
Non-Technical Title: Antioxidant Status and the Progression of Glaucoma
Duration: April 1, 2010 - July 31, 2012
Co-PI(s):
Christopher Reilly, The Regents of the University of California-Davis
Summary: The capacity of trabecular meshwork cells to resist oxidative stress is reduced in glaucoma. Research to investigate this loss in protection of the cells has disregarded the importance of biophysical cues in contributing to the antioxidant status. This study examines the contribution of nanoscale surface features and biomechanics to the total antioxidant status of these cells.
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Program: Glaucoma
Award Type: Standard
$100,000
Brian C. Samuels, M.D., Ph.D.
Trustees of Indiana University
Indiana, IN, United States
Title: Hypothalamic Control of Translaminar Pressure Gradients
Non-Technical Title: How the Brain Controls Changes in Eye Pressure and Brain Pressure
Duration: July 1, 2011 - June 30, 2013
Summary: For a long time, scientists believed that glaucoma was caused by damage to the nerve in the back of the eye when the pressure inside the eye was too high. Recently, there has been new evidence that pressure inside the brain is also important. We will focus on finding out how the brain controls the pressure in the eye and the brain in an attempt to find new treatment options for patients with glaucoma.
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Program: Glaucoma
Award Type: Standard
$100,000
Joel Schuman, M.D.
University of Pittsburgh
Pittsburgh, PA
Title: Spectral Domain OCT Doppler Assesses Aqueous Outflow
Non-Technical Title: A New Non-Contact Measurement of the Process that Controls Eye Pressure
Duration: April 1, 2010 - September 30, 2012
Co-PI(s):
Larry Kagemann, M.S., Gadi Wollstein, M.D., Hiroshi Ishikawa, M.D.
University of Pittsburgh
Haiyan Gong, M.D., Ph.D.
Boston University
Summary: The most important factor to consider in glaucoma is the pressure of the eye, which is controlled by the slow outflow of fluid within a drainage system in the front of the eye. We have developed a way to visualize and measure how fast this drainage occurs without touching the eye, and without any bright lights. This project is vital in two ways: 1- in order to validate the new measurement in a controlled environment designed to be nearly identical to that of the clinic, and 2- in order to finally visualize, for the first time, the entire system as it functions.
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Program: Glaucoma
Award Type: Standard
$100,000
Arthur Sit, M.D.
Mayo Clinic College of Medicine
Rochester, MN
Title: Characterization of Episcleral Venous Pressure in Humans
Non-Technical Title: Measuring pressure in the eye's veins: a key to understanding glaucoma
Duration: April 1, 2010 - March 31, 2013
Co-PI(s):
Jay McLaren, Mayo Clinic College of Medicine
Summary: Measurement of episcleral venous pressure is critical to understanding the changes in intraocular pressure that occur in normal and glaucomatous eyes, but no reliable method has previously been available for human use, resulting in an incomplete understanding of aqueous humor dynamics. We have developed a new technique and device to allow precise and accurate measurement of episcleral venous pressure by providing reproducible measurement endpoints. In this project, we further develop the technique and analysis software so that it is suitable for large scale projects, enabling future investigations into episcleral venous pressure and aqueous humor dynamics in normal subjects and glaucoma patients.
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Program: Glaucoma
Award Type: Standard
$100,000
Alexander C. Theos, Ph.D.
Georgetown University, School of Nursing & Health Studies
Washington, DC, United States
Title: Cell Biology of NMB in Pigmentary Glaucoma
Non-Technical Title: Cellular Function of a Protein, NMB, Important in Eye Disease
Duration: July 1, 2012 - June 30, 2014
Summary: DBA/2J mice are an animal model of pigment dispersion syndrome (PDS), which is a precursor to glaucoma in humans. These mice are thought to have a loss-of-function mutation in the NMB gene that is responsible for this disease. Dr. Theos and colleagues are proposing experiments that will characterize the NMB protein within pigmented cells of the eye in order to understand how NMB functions in normal cells, and, in addition, how loss of function of NMB causes PDS.
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Program: Glaucoma
Award Type: Standard
$100,000
Derek S. Welsbie, M.D., Ph.D.
Johns Hopkins University, School of Medicine
Baltimore, MD, United States
Title: Genome-wide RNAi Screening in Retinal Ganglion Cells
Non-Technical Title: Identifying New Drug Targets in Glaucoma
Duration: July 1, 2012 - June 30, 2014
Summary: Vision loss from glaucoma is caused by the death of retinal ganglion cells, important nerve cells which carry vision from the eye to the brain. Dr. Welsbie and colleagues are using gene therapy to better understand the signals that trigger the death of these ganglion cells. In doing so, these researchers hope to identify new drug targets that could be used to prevent cell death and vision loss.
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Program: Glaucoma
Award Type: Standard
$100,000
Shunbin Xu, M.D., Ph.D.
Rush University Medical Center
Chicago, IL, United States
Title: MicroRNAs in Glaucomatous Neurodegeneration
Non-Technical Title: microRNAs in glaucoma
Duration: July 1, 2011 - June 30, 2013
Summary:
- microRNAs are newly recognized regulators of gene expression, playing important roles in both normal functions and diseases in almost all organ systems.
- Glaucoma is the result of malfunction and death of retinal ganglion cell.
- This research will identify the microRNAs involved in the malfunction and death of retinal ganglion cells during the development of glaucoma, which may be novel therapeutic targets for the treatment of the disease.
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Program: Glaucoma
Award Type: Standard
$100,000
Zhiyong Yang, M.D., Ph.D.
Johns Hopkins University
Baltimore, MD, United States
Title: Role of a Protein Kinase in Retinal Ganglion Cell Degeneration in Glaucoma
Non-Technical Title: A Novel Target in Promoting Retinal Ganglion Cell Survival in Glaucomain Glaucoma
Duration: July 1, 2012 - June 30, 2014
Co-PI(s):
Donald J. Zack, M.D., Ph.D.
Johns Hopkins University
Summary: The research proposed in this application will directly determine the potential value of a new protein target in the treatment of vision loss in glaucoma. In addition, Drs. Yang, Zack, and colleagues will evaluate a drug candidate that can block this target for its potential to preserve vision in a rodent model of glaucoma.
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Program: Glaucoma
Award Type: Standard
$100,000