Therapy Analysis - AMD
The causes of age-related macular degeneration
Age–related macular degeneration (AMD) accounts for nearly 50% of all visual impairment in the developed world. It is associated with adults over the age of 50, and is characterized by thinning and atrophy of the macula, an area of the retina responsible for detailed vision. In advanced cases bleeding and scarring may also occur.
The National Eye Institute estimates that there are 1.7 million people with the advanced form of AMD in the US alone and that this number will grow to 3 million by 2020. AMD is painless and patients with early stages of the disease often have little or no symptoms. However, as the disease progresses central vision is gradually lost, leaving a dark, greyish or distorted patch in its place. An important clinical hallmark of AMD is the presence of drusen, yellow or off-white accumulations of extracellular material on the choroid, which are present in increasing size and number as AMD progresses. Although it is understood that this increase in drusen indicates a more advanced stage of AMD, it remains unclear as to whetherdrusen act to promote AMD or are simply symptomatic of the cause of AMD. It is easy to underestimate the impact of this loss of visual function over time. Indeed, patients often comment that pictures attempting to represent this visual loss merely as a blurred spot do not do justice to the debilitating nature of AMD. It has drastic implications on patient's ability to perform everyday tasks such as driving, reading, recognizing faces and even identifying food on a plate in front of them.
AMD is classified into two forms: dry AMD (central geographic atrophy) and wet AMD (neovascular). The dry form accounts for 90% of all AMD diagnosed and is caused by the gradual degeneration of photoreceptor cells in the macula. In healthy eyes, photoreceptor cells are dependant on a single layer of pigmented cells lying between the macula and the choroid, known as retinal pigmented epithelium (RPE) cells. RPE cells mediate the transfer of nutrients and oxygen from blood vessels in the choroid to the photoreceptor cells and the subsequent removal of metabolites and debris. Patients with dry AMD lack a fully functioning RPE, resulting in an accumulation of debris and depletion of nutrients in photoreceptor cells. With the persistence of such conditions, photoreceptor cells die, resulting in the thinning and atrophy of the macular, and thus the depletion of central vision characteristic of AMD. Many people with early dry AMD will have no noticeable difference in their vision; however, as the disease progresses sufferers report difficulties seeing at night, decreased reading vision, blurring that goes away with brighter lighting and by the time the disease reaches the advanced stages, the complete loss of central vision.
The development of wet AMD is heavily associated with the dry form of the disease, with 10% of those with dry AMD developing wet AMD at some stage, often occurring rapidly and without warning. This is the more visually debilitating form of the disease and is responsible for more than two thirds of all vision loss associated with AMD. Wet AMD is characterized by the abnormal growth of new blood vessels under the macula, in a process known as choroid neovascularisation (CNV). These new vessels are often very fragile and leak blood or fluid into the tissue at the back of the eye, detaching the retina from the RPE in a blister and causing scarring and permanent damage to the macula. In addition to the visual disturbances previously mentioned, wet AMD patients also describe difficulties seeing the borders between objects or 'washed out' eyesight. Colours can appear less bold and the ability to tell the difference between them is hampered. Many also experience distorted vision, for example the straight line of a doorframe or table top looks wavy or crooked. Scotomas, shadows and missing areas, develop and central vision is rapidly lost.
