Scientists have identified a new target for the diagnosis and treatment of age-related macular degeneration (AMD). AMD most commonly affects people over the age of fifty and is the leading cause of vision loss in those over sixty. The rarer, but more serious form of the disease, wet AMD, is caused by abnormal blood vessel growth under the macula (centre of the retina) and can develop very quickly. Although the condition is painless, the new blood vessels leak blood and fluid which lift the macula and destroy sharp central vision. The condition can be treated with laser surgery, photodynamic therapy or anti-vascular endothelial growth factor (anti-VEGF) injections into the eye, although none of these treatments provides a complete cure and loss of vision may continue despite treatment.

The new study, published online on Jun 14^th in Nature, shows that blocking the eosinophil/mast cell chemokine receptor, CCR3, can reduce the abnormal blood vessel growth that leads to AMD. The researchers detected CCR3 protein in eye tissue from people with AMD but not in eye tissue from people of the same age who did not have the disease. In studies in mice, blocking CCR3, either by genetic engineering or using antibodies, reduced the number of abnormal blood vessels. In the mice, targeting CCR3 was shown to be more effective than targeting VEGF (70% vs 60%), suggesting that CCR3 blockers could also provide an effective treatment for patients with AMD. The team injected anti-CCR3 antibodies attached to semiconductor nanocrystals into mice and, using conventional ocular angiography techniques, were able to visualise the abnormal blood vessels even before they had penetrated the retina. Since CCR3 was detected at an early stage in the development of the disease, the researchers hope that the new imaging technology could be used diagnostically, and that early detection will provide better opportunities to prevent structural damage and preserve vision.

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Age-Related Macular Degeneration (AMD) is a condition in which the centre of the retina (the macula) gradually deteriorates, and the detailed vision needed for reading, driving and recognizing faces is lost. There are two types of AMD, a dry form and a wet form: the dry form is more common, but less severe, than the wet form. In the dry form, the cells don’t take in enough vital nutrients and fail to clear cellular by-products so that eventually photoreceptors are lost from the central part of the eye. The wet form is characterised by the growth of new blood vessels which can bleed and leak fluid, leading to scarring and more rapid loss of vision. There is currently no specific treatment for dry AMD, whilst treatment for the wet form involves laser treatment to seal the leaking blood vessels or injection of anti-vascular endothelial growth factor (anti-VEGF) drugs directly into the eye.

A report in the New England Journal of Medicine now warns that a new treatment being developed for the treatment of wet AMD may actually cause harm in patients with the dry form of the disease. The new treatment, which is currently undergoing clinical trials, uses interfering RNA (RNAi) technology to downregulate production of VEGF or VEGF receptors. The new study identifies a link between toll-like receptor 3 (TLR3), which helps the immune system to recognize viral infections, and dry AMD. A mutation associated with low activity of TLR3 appears to offer protection against dry AMD, possibly by suppressing death of retinal cells. The use of RNAi induces TLR3 activation, and so could worsen the prognosis in patients with dry AMD. The discovery also suggests that TLR3 inhibitors may offer a potential new treatment for the more common, dry, form of AMD.

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