National Glaucoma Research - Current Awards Julie Albon, Ph.D.Cardiff University Title: Discs at Risk: Novel Optic Nerve Head Phenotyping in Glaucoma Co-PI(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 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. Program: Glaucoma  Michael Julien Alexandre Girard, Ph.D.Imperial College London Title: In Vivo Corneal Biomechanics: A Biomarker for Glaucoma? 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. Program: Glaucoma  David J. Calkins, Ph.D.Vanderbilt University Medical Center Title: Mapping the Protein and Lipid Signature of Glaucoma Co-PI(s):
Kevin Schey, Ph.D.
Vanderbilt University 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. Program: Glaucoma  Peter P. De Deyn, M.D., Ph.D.Institute Born-Bunge Title: Cerebrospinal Fluid Pressure At The Link Between Glaucoma And Alzheimer’s Disease 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. Program: Glaucoma  Chad A. Dickey, Ph.D.University of South Florida Title: Disrupting Chaperone/Myocilin Complexes for Glaucoma 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. Program: Glaucoma  Michael Fautsch, Ph.D.Mayo Clinic College of Medicine Title: Role of intracranial hypotension on optic neuropathy 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. Program: Glaucoma  Gareth Howell, Ph.D.The Jackson Laboratory Title: Characterizing the Endothelin System in Glaucoma Co-PI(s):
Simon John, The Jackson Laboratory
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. Program: Glaucoma  Paul A. Knepper, M.D., Ph.D.University of Illinois at Chicago Title: Activation of Innate Immune Toll-4 Receptor in POAG 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. Program: Glaucoma  Peter Koulen, Ph.D.University of Missouri at Kansas City Title: Protection of ONH astrocytes and structure in glaucoma Summary: Degeneration or acute damage of the retina due to glaucoma related disease processes is a major cause of visual loss and blindness in the United States and worldwide. As glaucoma affects significant and increasing portions of the U.S. population including minorities affected by disparities in health care delivery, determining causes, mechanisms of action and subsequently potential treatment strategies will contribute to improving health care, health and performance requiring visual tasks. This study uses a novel mechanism underlying a self-defense mechanism of the retina to protect a critical structure of the retina, the optic nerve head, in order to develop new treatment strategies that have the potential to be complementary in nature to current strategies aimed at neuroprotection or aimed at lowering intraocular pressure. Program: Glaucoma  John Kuchtey, Ph.D.Vanderbilt University Medical Center, Vanderbilt Eye Institute Title: Identification of Glaucoma Genes by Exome Sequencing Co-PI(s):
Rachel W. Kuchtey, M.D., Ph.D.
Vanderbilt University Medical Center Summary: The purpose of this study is to identify disease-causing gene(s) in two families with inherited primary congenital glaucoma (PCG). These families have already been screened for genes known to cause PCG, and no causative mutations were found. Therefore, identifying the disease-causing mutations in these families will result in the discovery of new glaucoma genes. Program: Glaucoma
Last Review: 04/29/13 |
BrightFocus Foundation |
