Major breakthrough in early detection and prevention of AMD

The research team discovered that CCR3 not only provides a unique signature for CNV, but the gene actively promotes the growth of these abnormal blood vessels in the eye. Thus the same anti-CCR3 antibodies used to detect CNV could potentially be useful as a clinical treatment to prevent macular degeneration.

The early results look promising. Treatment with anti-CCR3 antibodies reduced CNV in mice by about 70 percent, as opposed to 60 percent with VEGF-based treatments currently in clinical use. Ambati says Phase I clinical trials are not far off.

"The identification of CCR3 on the endothelial cells of CNV in human AMD is a major breakthrough," said Dr. Patricia A. D'Amore, professor of ophthalmology at Harvard Medical School. "The preclinical data is very exciting and suggests that targeting CCR3 may be the basis of the next generation of targeted anti-angiogenesis therapy for wet AMD."

Ambati's paper, "CCR3 is a target for age-related macular degeneration diagnosis and therapy," was released online today and will be printed in an upcoming issue of Nature.

Age-related macular degeneration is the leading cause of blindness in older adults in the industrialized world, affecting some 10-12 million people in the United States – more than all cancers combined and about twice as many as Alzheimer's disease. Nationwide, about 250,000 new cases of CNV are reported annually.

This work was supported by research grants from the National Eye Institute of the National Institutes of Health and an unrestricted grant from Research to Prevent Blindness. Dr. Ambati is also supported by a Doris Duke Distinguished Clinical Scientist Award and the Burroughs Wellcome Translational Research Clinical Scientist Award. Key collaborators in the study include Drs. Marc Rothenberg (Cincinnati Children's Hospital), M. Elizabeth Hartnett (UNC-Chapel Hill), Craig Gerard (Children's Hospital, Boston), Salvatore Grisanti (University of Luebeck), and Justine Smith (Casey Eye Institute).