Defective proteostasis is one of the hallmarks of aging cells and tissues. Of the different components of the proteostasis network, we are interested in autophagy and its changes with age in retina. We have previously shown that, out of the different autophagic pathways that co-exist in all mammalian cells, macroautophagy is the first that declines with age in the retina. A crosstalk between macroautophagy and chaperone mediated autophagy (CMA) has been described whereby, in aged mice retinas, the decrease in macroautophagy correlates with increased CMA. Our working hypothesis is that aged and degenerated retinal cells increase CMA to compensate for macroautophagy loss, in an attempt to maintain cell viability. To test our hypothesis, we use histological and biochemical analysis, but also functional read outs as electroretinogram (ERG) or optic coherence tomography (OCT) and visual behavioral tests. If proven correct, increasing CMA and other selective autophagy pathways such as mitophagy could be a potential treatment to delay consequences of aging in the retina and to ameliorate degeneration in neurodegenerative and age-related retinal pathologies.