The maintenance of protein homeostasis, or proteostasis, is crucial for the proper functioning of cells. Proteostasis refers to the cycle of synthesizing, folding, transporting, and degrading proteins. The main site of protein synthesis within the cell is the endoplasmic reticulum (ER). When protein folding load is excessive, proteostasis is disrupted and ER stress ensues. Activation of the unfolded protein response (UPR) pathway acts to reduce ER stress and restore proteostasis. However, with age the UPR becomes less efficient, or even maladaptive, contributing to sleep deficits and cognitive impairments. As the number of aged individuals in the population grows due to the advances of modern medicine, so does the incidence of age-related disorders. Age is a major risk factor for the development of Alzheimer’s disease (AD). Cognitive dysfunction and sleep deficits are prominent features of AD, coupled with protein dyshomeostasis in the form of protein aggregates such as Aβ plaques. Further, protein synthesis is necessary for memory formation, and disruptions in proteostasis can have direct consequences for cognition in both age and disease. Given this, it remains unclear if there is a causal link between proteostasis, sleep quality, and cognition across aging and disease. In the following dissertation, we use a mouse model of aging and a mouse model of Alzheimer’s disease to determine if reducing ER stress via increasing protein chaperone levels, either systemically via intraperitoneal PBA injections or locally via hippocampal microinjections with an AAV-BiP, improves both sleep quality and memory. Our results suggest that chaperone treatment consolidates sleep in a wildtype mouse model of aging and improves learning in both a mouse model of aging and AD. Chaperone treatment reduces ER stress in both models and leads to an increase CREB activity which is linked to improved cognition. Further, chaperone treatment in a mouse model of AD led to the increase of XBP1s and ADAM10, which are associated with the non-amyloidogenic cleavage of APP. The implications of these results could have an impact on the development of therapies to improve healthspan in the growing aged population and inform the development of potential treatments for Alzheimer’s disease.