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Julie Albon, Ph.D.
Cardiff University
Cardiff, Wales
Title:
Discs at Risk: Novel Optic Nerve Head Phenotyping in Glaucoma
Non-Technical Title:
A Quantitative Index that Characterizes Optic Nerves at Risk of Glaucoma
Duration:
July 1, 2011 - June 30, 2013
Co-Investigator(s):
Wolfgang Drexler, Ph.D.
Medical University Vienna
Michael Girard, Ph.D.
Imperial College, London
James Morgan, D.Phil., FRCOphth, Rachel North, Ph.D.
Cardiff University, Wales
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Summary: The lamina cribrosa is a structure in the optic nerve that is altered in glaucoma, resulting in vision loss. The aim of this project is to identify early signs of changes in lamina cribrosa integrity before nerve fibers are damaged and vision is lost. These signs will be used to determine a novel quantitative index that will be used to determine which optic nerves are at risk of developing disease.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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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 - June 30, 2013
Co-Investigator(s):
Nick Strouthidis, MBBS, M.D., MRCOphth
Moorfields Eye Hospital
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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
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David J. Calkins, Ph.D.
Vanderbilt University Medical Center
Nashville, TN, United States
Title:
Mapping the Protein and Lipid Signature of Glaucoma
Non-Technical Title:
Molecular Changes Underlying Vision Loss in Glaucoma
Duration:
July 1, 2011 - June 30, 2013
Co-Investigator(s):
Kevin Schey, Ph.D.
Vanderbilt University
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Summary: Vision loss in glaucoma involves death of the optic nerve through unknown changes in the composition of the retina and nerve. Our studies will measure how elevated pressure in the eye causes compositional changes in the retina and optic nerve by imaging specific groups of molecules in intact tissue. This will help us identify new targets for potential treatments.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Michael Fautsch, Ph.D.
Mayo Clinic College of Medicine
Rochester, MN
Title:
Role of intracranial hypotension on optic neuropathy
Non-Technical Title:
Decreased intracranial pressure and glaucoma
Duration:
April 1, 2010 - March 31, 2012
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Summary: The proposed study will develop an animal model of decreased intracranial pressure and examine whether the lowering of intracranial pressure has a role in the development of glaucoma-like changes in the optic nerve and retinal ganglion cells.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Jeffrey Goldberg, M.D., Ph.D.
University of Miami Miller School of Medicine
Miami, FL
Title:
Manipulating Kruppel-Like Factors for RGC Regeneration
Non-Technical Title:
Enhancing optic nerve regeneration with gene therapy
Duration:
April 1, 2010 - March 31, 2012
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Summary: As a result of glaucoma, retinal ganglion cells (RGC) axons are damaged in the optic nerve head, and fail to regenerate through the optic nerve. Here we study methods to enhance RGCs' intrinsic capacity for optic nerve regeneration through manipulation of the “KLF” family of transcription factors using a gene therapy approach. Enhancing optic nerve regeneration may enhance recovery from glaucomatous optic nerve damage.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Daniel Goldman, Ph.D.
The Regents of the University of Michigan
Ann Arbor, MI
Title:
Müller glia-dependent regeneration of retinal ganglion cells
Non-Technical Title:
Retinal ganglion cell regeneration for retinal repair
Duration:
April 1, 2010 - March 31, 2012
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Summary: This research aims to test the hypothesis that retinal ganglion cell death stimulates “Müller glia” dedifferentiation into a population of proliferating retinal progenitors that can regenerate lost retinal ganglion cells. We propose to use zebrafish in these studies because of their robust regenerative powers. Our approach is to first generate a transgenic zebrafish model of retinal ganglion cell death, similar to that which occurs during glaucoma, and then investigate if Müller glia can regenerate these damaged cells.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Gareth Howell, Ph.D.
The Jackson Laboratory
Bar Harbor, ME
Title:
Characterizing the Endothelin System in Glaucoma
Non-Technical Title:
Determining the importance of Endothelins in glaucoma
Duration:
April 1, 2010 - March 31, 2012
Co-Investigator(s):
Simon John,
The Jackson Laboratory
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Summary: No therapies are available that target neuronal death in glaucoma. Here, we assess an important pathway, the Endothelin System, to better understand the mechanisms of neuronal cell death. Endothelins are normally thought to influence, blood pressure. However, this work could lead to the development of improved therapies for human glaucoma.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Mark Johnson, Ph.D.
Northwestern University
Evanston, IL
Title:
Biomechanical Characterization Of SC Cells
Non-Technical Title:
Cell Stiffness In Glaucoma
Duration:
April 1, 2009 - March 31, 2012
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Summary: Are the cells of the inner wall of Schlemm's canal stiffer in glaucomatous eyes than in normal eyes? If so, is this stiffness change responsible for the elevated intraocular pressure characteristic of glaucoma.
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Program: Glaucoma
Award Type: Standard
$84,197
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Jeffrey Kiel, Ph.D.
The University of Texas Health Science Center at San Antonio
San Antonio, TX
Title:
Regulation of episcleral venuos pressure
Non-Technical Title:
Is a key controller of intraocular pressure regulated?
Duration:
April 1, 2010 - March 31, 2012
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Summary: Episcleral venous pressure (EVP) is a primary cause of intraocular pressure (IOP), yet we know little about it. The episcleral blood vessels have nerves, which suggests that EVP is regulated, but we do not know if failure of EVP regulation causes high IOP, or if we can lower EVP with drugs as a new way to treat glaucoma. This project seeks to shed light on the answers to these questions.
More details
Program: Glaucoma
Award Type: Standard
$100,000
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Paul A. Knepper, M.D., Ph.D.
University of Illinois at Chicago
Chicago, IL, United States
Title:
Activation of Innate Immune Toll-4 Receptor in POAG
Non-Technical Title:
Activation of Innate Immunity System and Gluacoma
Duration:
July 1, 2011 - June 30, 2013
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Summary: We have identified a unified signaling pathway based on activation of innate immune system which results in an inflammatory cascade resulting in POAG. We have identified that cell trauma causes low-molecular-weight hyaluronic acid to start the pathway. Prevention of degradation of high-molecular-weight hyaluronic acid by potent hyaluronidase inhibitor could be novel therapy and the first therapy directly aimed at the cause of POAG.
More details
Program: Glaucoma
Award Type: Standard
$100,000
