Investigators at the University of North Carolina and University of Kentucky have identified a new target allowing for the early detection and early treatment of macular degeneration. With macular degeneration being the most common cause of blindness in the elderly, having a method for early detection and subsequently early prevention of this eye disease is exciting.
Researchers have identified that blocking the protein known as CCR3 can reduce the abnormal blood vessel growth that causes macular degeneration. Targeting this new protein may prove both safer and more effective than current macular degeneration treatments.
Current macular degeneration treatments are directed at a protein called vascular endotheilial growth factor (VEGF). Current macular degeneration anti-VEGF drugs may pose risks of blocking the growth of healthy blood vessels in healthy areas of the body, not just the abnormal blood vessels associated with the eye disease.
The new discovery may enable physicians to detect macular degeneration in its earliest stages before abnormal blood vessels have fully affected the macula and cause vision loss. Preventing macular degeneration at this early stage would be much better than treating the eye disease with drugs. According to Mary Elizabeth Harnett, M.D., a professor of ophthalmology in the UNC School of Medicine, “An exciting implication of this study was that CCR3 protein could be detected in early abnormal blood vessel growth, giving us the opportunity to prevent structural damage to the retina and preserve vision.”
With macular degeneration estimated to affect 30 to 50 million people worldwide with the number expected to double in the next 10 years, early detection and prevention of the eye disease is crucial.
Macular degeneration is currently treated with anti-VEGF drugs such as Lucentis, Macugen, and Avastin. However, as previously stated, blocking the VEGF protein can also damage healthy blood vessels in healthy portions of the body. Using the CCR3 protein to detect and develop new macular degeneration treatments that specifically target the eye disease.
The presence of the CCR3 protein is detected in people with macular degeneration but not in people who do not have the eye disease. When researchers blocked the CCR3 protein there was a reduction in the generation of abnormal blood vessels. Drugs targeting the CCR3 protein associated with macular degeneration were significantly more effective than those targeting the VEGF protein. This could signal an increase in treatment options for patients suffering from the eye disease where approximately two-thirds of macular degeneration patients do no respond to existing VEGF treatments.
Researchers are now determining whether the levels of the CCR3 protein in the bloodstream can be used to assess risk associated with developing macular degeneration.