A decrease in the rate of protein turnover and the intracellular accumulation of altered proteins in cytosol and membranes are features common to all aged cells. Diminished autophagic activity plays a major role in these age-related manifestations. In this work we review the molecular defects responsible for the malfunctioning of two forms of autophagy - macroautophagy and chaperone-mediated autophagy - in old mammals, and highlight general and cell-type specific consequences of dysfunction of the autophagic system with age. Dietary caloric restriction and antilipolytic agents have been proven to efficiently stimulate autophagy in old rodents. These and other possible restorative efforts are discussed.