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The goal of the Catalyst for a Cure (CFC1) research team is to find the earliest cellular events in glaucoma progression and to develop potential new therapies that directly target degeneration of the retina and optic nerve in the disease.
In 2011, The CFC researchers focused on developing a novel and therapeutically important concept in glaucoma. Converging sets of experimental results indicate that in the most prevalent forms of glaucoma, there is no single event that accounts for degeneration of the retina and optic nerve. Rather, multiple injuries arising from eye pressure overwhelm naturally protective pathways and unleash a chain of events that eventually leads to blindness.
CFC1 research indicates that the onset and speed of vision loss in glaucoma depends upon a critical “tipping point.” In healthy eyes, the retina and optic nerve are able to adapt to small changes in ocular pressure. The eye accomplishes this through the actions of chemical pathways that heal minor injuries over the course of a lifetime.
This “healing” response requires the ability to acquire new cellular energy and discharge harmful byproducts caused by increased demand and metabolism. The retina and optic nerve have specialized cells that manage these byproducts to prevent harmful accumulation.
The tipping point involves a delicate balance between the metabolism of the retina and optic nerve, communication between individual cells necessary to monitor and influence metabolism, and the maintenance of the tissue by cells that dispose of waste. Vision loss is likely in glaucoma when this balance is disturbed at a fast pace.
By monitoring cellular communication using specialized biomarkers that can be seen in the living eye, the CFC was able to track the onset of glaucoma very early to pinpoint exactly when the balance was disturbed. By manipulating the chain of events arising from cells under stress and blunting their response, the CFC found it could tip the balance in favor of survival of the retina and optic nerve even when eye pressure was high. To do this, the CFC developed several new experimental tools, including the ability to determine if new approaches to therapy could actually enhance vision.
The CFC’s ideas, tools and results are fundamentally changing how the scientific and medical communities view vision loss in glaucoma. It is the CFC’s hope that the work accomplished in 2011 will lay the foundation for detection of glaucoma at its earliest stages, and for new drug therapies to slow or stop degeneration of the retina and optic nerve in the disease.
David J. Calkins, PhD Vice-Chairman and Director of Research; Professor of Ophthalmology and Visual Sciences, Neuroscience and Psychology, Vanderbilt Eye Institute, Nashville, Tennessee
Philip J. Horner, PhD Associate Professor, Department of Neurological Surgery
Institute for Stem Cell and Regenerative Medicine, University of Washington, Seattle, Washington
Nicholas Marsh-Armstrong, PhD Assistant Professor, Departments of Ophthalmology and Neuroscience, Johns Hopkins School of Medicine, Kennedy Krieger Institute, Baltimore, Maryland
Monica L. Vetter, PhD Neurobiology and Anatomy Department Chair, George and Lorna Winder Professor of Neuroscience, University of Utah, Salt Lake City, Utah
First posted May 1, 2012
Last reviewed on June 10, 2021