Abstract
As the organism ages, there is a decline in effective energy supply, and this retards the ability to elaborate new proteins. The consequences of this are especially marked in the gradual decline in brain function. The senescence of cells and their constituent organelles is ultimately the cause of aging of the entire nervous system. What is less immediately obvious is that brain aging is also accompanied by the failure of catabolic events that lead to the removal of non-functional cells and ineffective subcellular components. The removal of non-working cellular and subcellular elements within the brain is essential in order to allow the appearance of fresh cells and organelles with a full range of capacities. Thus, the maintenance of operative mechanisms for the dispersal of failed tissue components is important, and its diminished capacity with aging is a significant contributory factor to the onset and progression of age-related neurological disorder. This report discusses the mechanisms underlying autophagy and phagocytosis and how these can be adversely modulated as aging proceeds. The means by which the effective recycling of cellular components may be reinstated in the aged brain are considered.