Age-related macular degeneration (AMD) is a highly prevalent macular condition that primarily affects the older population. It is the primary cause of blindness amongst the elderly population. It is an inflammatory disease that characteristically shows choroidal neovascularization and geographic atrophy. The exact pathomechanism of developing AMD is not known. However, certain factors such as increased age, smoking, genetic factors and certain environmental factors are usually associated with the development of the disease. AMD also involves oxidative stress-mediated destruction of retinal pigment epithelial cells and, consequently, that of retinal photoreceptors. Alzheimer's disease (AD) is a degenerative disorder involving the nervous system that usually affects people aged 65 and over. Both AMD and AD are age-related, degenerative conditions that have several similarities and share many of the same risk factors such as vascular conditions like arteriosclerosis, high blood pressure and obesity. It is believed that the early emergence of the clinical manifestations of AMD and AD may also be significantly influenced by oxidative stress and genetic polymorphism in complement factor H. A common pathogenic pathway between AD and AMD is quite likely. Amyloid-β is an aberrant protein that accumulates within the brains of Alzheimer's patients and appears as plaques on magnetic resonance imaging (MRI). These plaques are a pathognomonic sign of Alzheimer's disease. Similar to this, amyloid-β deposits are reported to build up beneath the retina of AMD patients, which appear as tiny clusters of protein-lipid substances known as drusen. It has also been found that individuals suffering from AMD exhibit an increased chance of developing AD than those with no AMD.
Keywords: choroidal neovascularization; drusen; geographic atrophy; retinal pigment epithelium (rpe); vascular endothelial growth factor (vegf).
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