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The second serious vision problem is age-related macular degeneration (AMD). AMD is the leading cause of acquired blindness and vision impairment among elderly Americans. It is estimated that up to 17 million elderly have at least early signs of this disease called, Age Related Maculopathy (ARM). These patients have early symptoms noticeable only by an eye exam. The NEI estimates that nearly 1.7 million elderly Americans have the more advanced stages of AMD and a new case is diagnosed every 3 minutes (up to 500,000 new diagnoses/yr) The prevalence increases with age affecting one in six Americans aged 55-64 rising to one in three in Americans over 75. Of the 1.7 million currently afflicted the most prevalent form is called Dry AMD accounting for nearly 85% of the cases.
Patients who are affected have gradual loss of central vision due to the death of photoreceptor cells (rods and cones) and their close associates; retinal pigmented epithelium (RPE) cells. Photoreceptors, the cells in the retina that actually "see" light, are essential for vision. RPE cells are like the nursemaids for photoreceptor cells and are necessary for photoreceptor survival and functioning. Death of either of these cell types leads to death of the other. The cell death occurs in the macula. This is unfortunate because the macula contains the highest concentration of cone-type photoreceptors which are responsible for providing color and fine detail in the center of the visual field. Therefore, patients with AMD gradually lose their central vision, and with it the ability to drive, read, and see faces of loved ones. As bad as this may seem, it is a gradual process and is compatible with reasonable functioning for many years.
However, there is another aspect of AMD that is even more devastating. As the photoreceptor and RPE cells slowly degenerate, there is a tendency for blood vessels to grow from normal location in the choroid into an abnormal location beneath the retina.
This abnormal new blood vessel growth is called choroidal neovascularization (CNV) or Wet AMD. This abnormal blood vessels leak and bleed, resulting in sudden and severe loss of central vision. Depending on the location, laser treatment can sometimes be given to destroy the blood vessels. New drugs are currently under development for the wet form.
When retinal cells are lost they are not replaced and central vision loss can be profound. Recently the NEI released a report of an intervention trial with dietary antioxidants that show promise for delaying the progression of late stage AMD (AREDS - Report #8, 2001). Two promising antioxidants, zeaxanthin and lutein, were not far enough along in development to be included in this NEI Trial. This review will explain why these two promising antioxidants are ready for major clinical intervention trials. |