Catalyst for a Cure was launched a decade ago as a novel initiative to advance basic science research on the pathophysiology of glaucoma, ultimately to lead to a cure. At Catalyst for a Cure: The Annual Benefit on Thursday evening, the four principal investigators provided an update on their progress in elucidating the molecular mechanisms of neurodegeneration in glaucoma and identifying promising targets for therapeutic interventions that can delay or prevent retinal ganglion cell loss.
San Francisco-Catalyst for a Cure (CFC) was launched a decade ago as a novel initiative to advance basic science research on the pathophysiology of glaucoma, ultimately to lead to a cure.
At Catalyst for a Cure: The Annual Benefit on Thursday evening, the four principal investigators provided an update on their progress in elucidating the molecular mechanisms of neurodegeneration in glaucoma and identifying promising targets for therapeutic interventions that can delay or prevent retinal ganglion cell loss.
David Calkins, PhD, vice chairman and director of research, and professor of ophthalmology and visual sciences, neuroscience, and psychology, Vanderbilt University, Nashville, TN, said a recent publication in the Proceedings of the National Academy of Sciences describes the exciting finding that some of the earliest detectable glaucoma-associated changes in the visual pathways involve more distal connections, between the optic nerve and the brain.
“Previously, research aimed at identifying early events had focused on broken connections between the retina and the optic nerve,” he explained.
Monica L. Vetter PhD, neurobiology and anatomy department chairwoman, George and Lorna Winder Professor of Neuroscience, University of Utah, Salt Lake City, said that her lab in collaboration with others in the CFC consortium have been concentrating on visualizing and tracking changes in the microglia.
“Success in this area has obvious clinical importance for the future because if we can develop methods to visualize microglia in vivo, we may be able to detect the onset of disease and monitor its progression over time,” she explained.
Philip J. Horner, PhD, associate professor, Department of Neurological Surgery, University of Washington, Seattle, spoke to the advantages of the consortium approach to research.
“It is rare to have a relationship such as this where labs can become interwoven together, and the functioning of this collaborative process has improved with time,” he said. “As a result, our scientific progress is advancing at a faster pace and the practical outgrowth has been that we have been able to publish some important findings that we believe have already influenced other researchers in the field.”
Nicholas Marsh-Armstrong, PhD, assistant professor of ophthalmology and neuroscience, Johns Hopkins University School of Medicine, Baltimore, noted the group has been surprised by the discoveries made over the past year because they represent brand new concepts about the biology of glaucoma. Looking ahead, he is encouraged about the implications of their findings for the future.
“We believe the unique biology that is unfolding through our research is at the heart of what causes blindness in glaucoma,” he said. “Based on these revealing findings, conversations we have been having within the CFC consortium over just the past few months are laying the groundwork for a whole new approach to this disease.”
Dr. Calkins is also very excited about the potential for future breakthroughs. He noted the project has reached a critical stage in which the individual groups have begun to bring together their findings and ideas in order to develop a unifying theory on disease mechanisms.
“This is extremely exciting because once we have a theory that fits all the information together, we will be able to make predictions about the outcomes of experimental interventions,” Dr. Calkins said. “Moving forward from there, if research proves those predictions are correct, we are that much closer to having a cure for the neurodegeneration that underlies glaucoma.”
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