Promising New Treatment for Macular Degeneration
A new treatment for macular degeneration from researchers at the University of North Carolina School of Medicine holds promise for a highly effective way of treating the abnormal blood vessels associated with vision loss.
"We believe we may have found an optimized treatment for macular degeneration," senior study author Sai Chavala said via a press release, MD, director of the Laboratory for Retinal Rehabilitation and assistant professor of Ophthalmology and Cell Biology & Physiology at the UNC School of Medicine. "Our hope is that MDM2 inhibitors would reduce the treatment burden on both patients and physicians."
Background information from the study shows that as many as 11 million Americans have some form of macular degeneration, known as the most common cause of central vision loss in the world. In fact, those with the disease may find many daily activities including driving, watching television and reading particularly difficult.
The best treatment available for the problem is through an antibody called anti-VEBF that's injected into the eye. In order to receive treatment, patients must visit their doctor for a new injection every 4 to 8 weeks that can be particularly costly and time consuming.
"The idea is we'd like to have a long-lasting treatment so patients wouldn't have to receive as many injections," said Chavala, via the release. "That would reduce their overall risk of eye infections, and also potentially lower the economic burden of this condition by reducing treatment costs." Chavala practices at the Kittner Eye Center at UNC Health Care in Chapel Hill and New Bern.
The study concludes with the following, via the release: "While anti-VEGF works by targeting the growth factors that lead to leaky blood vessels, MDM2 inhibitors target the abnormal blood vessels themselves causing them to regress - potentially leading to a lasting effect.
"Chavala and his colleagues investigated the effects of MDM2 inhibitors in cell culture and in a mouse model of macular degeneration. They found that the drug abolishes the problematic blood vessels associated with wet macular degeneration by activating a protein known as p53. "p53 is a master regulator that determines if a cell lives or dies. By activating p53, we can initiate the cell death process in these abnormal blood vessels," said Chavala.
More information regarding the study can be found via the Journal of Clinical Investigation.