Retinal Changes in Age-Related Macular Degeneration

摘要

Age-related macular degeneration (AMD) constitutes the leading cause of legal blindness after 65 years of age in developed countries. Fuller knowledge of the etiology and pathogenesis of this disease is needed to advance its early diagnosis and its treatment. Retinal aging and AMD form part of a continual deterioration in which the transition between aging and illness is signalled by a vision loss. Classically, the retinal pigmentary epithelium (RPE) was thought to be the main agent causing AMD, but researchers are currently finding that many other factors are involved, notably genetic, vascular (hypertension, arteriosclerosis) and environmental (exposure to UV light and oxidative damage). In aging and AMD, alterations occur in the choriocapillaris, RPE and the Bruch's membrane, which leads to a chronic inflammatory response. These damages result in deposits (drusen and basal laminar deposits), which hamper the normal diffusion of nutrients to the retina, injuring the outer retina. This situation can trigger retinal-choroidal atrophy or neovascularization. The inner retina also undergoes alterations, which, with the loss of vessels and the thickening of basal vascular membranes as well as of the inner limiting membrane (ILM), can bring about retinal ischemia. This can in turn induce the retinal macroglia (Miiller cells and astrocytes) to reactivate and later die, and the disappearance of the macroglial cells could induced neuronal death in the inner retina. Retinal ischemia could provoke the migration of astrocytes and Mtiller cells towards the vitreous humour in search of a metabolic reserve, constituting epiretinal membranes. Despite the different hypotheses that seek to explain AMD, ischemia may be a major factor in the genesis of this pathology. The control of the risk factors and the habits that promote ischemia could help prevent the advance of this eye disease.