Evidence for an inflammatory process in age-related macular degeneration gains new support

Abstract

A ge-related macular degeneration (AMD) is a sight-threatening eye disease that affects large numbers of the human population over the age of 65. It is particularly prevalent in European countries and in the United States, which has a large population of European descent. However, its incidence is increasing in Japan, as well, for reasons that are not clear (1). Currently, it is estimated that 1.75 million individuals suffer from this disease in the United States, and 7 million are said to be “at risk” (2). The emotional and socioeconomic impact of AMD is large because of reading and driving impairment caused by this disease, which primarily affects central (straight on) rather than peripheral (side) vision. The disease involves the macula of the retina, a region ≈6 mm in diameter that lies within the central axis of vision. The macula has an abundance of densely packed, specialized neurons called photoreceptor cells (rods and cones) that receive the visual stimulus and initiate a complicated cascade of biochemical and ionic events (phototransduction) that begin the visual process. A stratum of cells called the retinal pigment epithelium (RPE), resting like a single layer of paving stones on a bed of extracellular matrix called Bruch's membrane, separates the photoreceptor cells from their blood supply in the choroid (middle layer) of the eye wall. It is within the RPE layer and Bruch's membrane that the mischief leading to AMD is thought to begin. Risk factors for AMD are well established from epidemiologic studies (3). In addition to advanced age, the risk factors include ocular pigmentation, dietary factors, a positive family history for AMD, high blood pressure, and smoking. Insights into the etiology of AMD have been slow in development because of the late onset of the disease. However, recent access to the human genomic sequence has …