Age-related maculopathy (or AMD) is the leading cause of new blindness in the U.S. population over age 60. Although the majority of AMD patients have the atrophic form of the disease, the major cause of severe vision loss in AMD is the exudative form. Recently, the Macular Photocoagulation Study reported that photocoagulation of choridal neovascular membranes, if performed at an early enough stage, can forestall vision loss from the exudative form of AMD. Consequently, it is important that AMD patients at high risk of developing exudative maculopathy be identified early and followed closely so that the choroidal membrane can be treated promptly. The search for risk factors has centered on drusen, the ophthalmoscopic hallmark of AMD. However, 30% to 50% of the population over age 60 have drusen, and only 1% to 5% per year of people with drusen develop the vision-threatening complications of AMD. At present, no satisfactory risk factors for vision loss from AMD have been identifed. Our research has shown that some people with drusen and normal visual acuity show large threshold elevations over the macula, similar to threshold elevations seen in AMD patients with exudative maculopathy, whereas most people with drusen show only small or no threshold elevations. Also, drusen patients exhibit contrast sensitivity changes that correlate with the grade of drusen. Our results suggest that retinal function measures may help to identify people with subclinical macular pathology from among the large group of people who have only drusen. To determine if retinal function measures can be used to identify high risk AMD patients, our team proposes to conduct 4 major research projects: 1) a 5-year prospective study of retinal function changes in unilateral drusen patients to determine if retinal function abnormalities are predictive of the development of exudative maculopathy; 2) a prevalence study of retinal function abnormalities among people who have only drusen and normal vision; 3) studies of retinal function changes in relation to retinal pathologic features of AMD; and 4) studies of the mechanisms of retinal function change in AMD.
NIH ExPorter
NIH ExPorter