A new target for the diagnosis and treatment of age-related macular degeneration (AMD) has been identified by an international scientific team. The researchers demonstrated that blocking the activity of a 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 VEGF. The researchers detected the presence of CCR3 in eye tissue from humans with AMD, but not in eye tissue from individuals of similar age who did not have the disease. When CCR3 activity was blocked in model systems, either with drugs or through genetic engineering, the researchers saw a decrease in the generation of abnormal blood vessels. Drugs targeting CCR3 were significantly more effective than those targeting VEGF, implying that targeting of CCR3 could represent a new therapy for the two-thirds of patients who do not respond to current treatment. AMD affects 30 to 50 million people around the world, and that number is expected to double in the next decade as the “baby boomer” generation ages. The discovery of the role of CCR3 may enable physicians to catch the disease at its earliest stages, before blood vessels have fully infiltrated and destroyed the central portion of the retina, an area known as the macula, to cause vision loss. "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,” said Dr. Mary Elizabeth Hartnett, one of the study authors.
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