Age-related macular degeneration (AMD) is a disease leading to severe visual loss and legal blindness in the population over 60 years of age. Its pathogenesis is likely multifactorial, involving a complex interaction of metabolic, functional, genetic, and environmental factors, and remains poorly understood. For these reasons, currently used therapeutic approaches are insufficiently effective. Although major abnormalities are seen in four functionally interrelated tissues, i.e. photoreceptors, retinal pigment epithelium (RPE), Bruch's membrane, and choriocapillaries, the impairment of RPE cell functions is an early and crucial event in the molecular pathways leading to clinical relevant AMD changes. The RPE progressively degenerates, which results in an irreversible degeneration of photoreceptors. Four processes: lipofuscinogenesis, drusogenesis, inflammation, and neovascularization, specifically contribute to the development of the disease. Two types of AMD are distinguished: the dry and the wet form. This paper briefly describes major molecular and cellular events leading to AMD, and presents currently used and new, forthcoming therapeutic strategies.