The life expectancy in the worlds population is increasing, highlighting the need of better understanding of the cellular and molecular pathways that drive the aging process. Because aging is the major risk factor to develop neurodegenerative conditions such as Alzheimers and Parkinsons disease, the number of patients affected is constantly increasing, representing a major social and economic problem. Importantly, abnormal protein aggregation is a transversal pathological event of most aging-related brain diseases, suggesting that the ability of neurons to handle alterations in the proteome is specifically altered (Kaushik and Cuervo, 2015). Several hallmarks of aging have been identified at the cellular and molecular level (Lopez-Otin et al., 2013; Kennedy et al., 2014), highlighting alterations in protein homeostasis or proteostasis. In fact, studies in simple model organisms indicate that the buffering capacity of the proteostasis network (PN) is reduced during aging (Douglas and Dillin, 2010; Mardones et al., 2015). The PN can be decomposed in different interrelated sub-networks including mechanisms responsible for protein synthesis, translation, folding, trafficking, quality control, secretion, and degradation (Balch et al., 2008). Sustained dysfunction of one or more components of the PN may translate into cell dysfunction and even proteotoxicity.