Age-related macular degeneration (AMD) causes loss of central vision and accounts for 50% of blind registration in the Western World. The incidence of AMD is expected to rise as a result of increased life span and changes in environmental factors. The aetiology of AMD is largely unknown. The lesions causing visual loss occur as a reaction to age-related changes at the outer retina where the retinal pigment epithelium, Bruch's membrane and choroidal vasculature is located. In the early stages of the disease, waste material (clinically identified as drusen) accumulates external to the retinal pigment epithelium, just internal to the choroidal inter capillary pillars in the Bruch's membrane. Drusen in the early stages of the disease do not generally affect vision, but their presence signals altered metabolic state and impaired clear-up function. The pigment of the retinal pigment epithelium may also become disturbed with areas of hyper- and hypo-pigmentation. The presence of drusen deposition and pigmentary changes are easy to identify clinically and intervention at this stage would be most desirable. At present, however, there are no medical interventions that could prevent the incidence or progression from the asymptomatic drusen only stage to end-stage disease with visual loss, largely because of the lack of knowledge on why and how early deposit formation occurs. The identification of the molecular steps leading to AMD is the focus of our research effort. We hope to identify novel pathways that will facilitate the development of early intervention strategies for the major cause of blindness in the elderly in Western societies. During ageing, there are changes in zinc homeostasis that induces frailty, general disability and increased incidence of age-related degenerative diseases like cancer, infections, atherosclerosis, Alzheimer's disease and this list now includes, based on our recent findings, AMD. Therefore, it is somewhat ironic that we know so little about zinc biology, especially in the retina, where the tissue concentration of zinc is the highest in the whole body. Recently we have published evidence of zinc being found in sub-retinal pigment epithelial deposits (that includes drusen and basal laminar and linear deposits) associated with AMD. This observation and the predictions we made based in that received tremendous international attention (see: http://news.bbc.co.uk/1/hi/health/6457427.stm). Currently we are gathering vital information to define the role zinc plays in the outer retina, and to understand how zinc controls the development and progression of AMD. Based on the role zinc plays in the two diseases and the many similarities between AMD and Alzheimer's disease we are also investigating the correlations between the two diseases.