Autophagy is the intracellular process that mediates the digestion of cellular components in lysosomes. The autophagic system fulfills two major functions in mammalian cells, serving both as an alternative source of energy, when nutrients are scarce, and as an efficient mechanism for the removal of any intracellular damage structure. Autophagic activity has been described to decline with age in almost all organisms and tissues, as wells as in several age-related disorders. On light of the prevalent functions of this catabolic process, cells with impaired autophagy are often energetically compromised and present severe problems in maintenance of cellular homeostasis and in the response to stress. Our group is interested in the study of the changes with age in different autophagic pathways and on the consequences of those changes in the aging organism. In addition, using both genetic manipulations and regulated diets, we have been able to prevent the decline in autophagic activity in old rodents and analyze the beneficial effect of this intervention both in cellular homeostasis and in their energetic balance. These models would help us evaluate the importance of maintaining proper autophagic function until advanced ages, and, on light of the observed cross-talk among autophagic pathways, the effect that repairing one autophagic pathway may have on the functioning of the others.