Researchers at the University of North Carolina at Chapel Hill School of Medicine in collaboration with lead investigators at the University of Kentucky have identified a new target for the diagnosis and treatment of age-related macular degeneration, the most common cause of blindness in older Americans.
In a study published online June 14, 2009 by the journal Nature, the researchers demonstrate that blocking the activity of a specific protein - called CCR3 -- can reduce the abnormal blood vessel growth that leads to macular degeneration. Furthermore, targeting this new protein may prove to be safer and more effective than the current treatment for the disease, which is directed at a protein called vascular endothelial growth factor or "VEGF."
The discovery -- made in mouse models and cultured human cells --may also enable physicians to catch the disease in its earliest stages, before blood vessels have fully infiltrated and destroyed the central portion of the eye's retina -- an area known as the macula -- to cause vision loss.
"It would be much better to prevent the disease in the first place," said study co-author and principal investigator of the UNC study site, Mary Elizabeth Hartnett, M.D., a professor of ophthalmology in the UNC School of Medicine. "An exciting implication of this study was that the 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."
Age-related macular degeneration (AMD) affects 30 to 50 million people globally, and that number is expected to double in the next decade as the baby boomer generation ages. The disease is currently treated with drugs that block the effects of VEGF, a growth factor that promotes the growth of abnormal blood vessels. However, because this factor is also involved in the growth and health of normal blood vessels, concerns have been raised about the safety of its long-term use. To date, however, these anti-VEGF agents have been found to be safe.