Aim: Lack of sleep has been linked in studies to increased beta-amyloid levels, oxidative stress, and memory impairments. Furthermore, sleep is known to help clear toxins that accumulate in the brain. This study investigated the restorative potentials of recovery sleep on total sleep deprivationinduced memory impairment, oxidative stress, stress response and changes in beta amyloid plaques in the hippocampus of adult male Wistar rats. Materials and Methods: Twenty-four male Wistar rats weighing between 150 and 200 g were divided into four groups. Group I remained in their home cages, while Groups II, III, and IV underwent sleep deprivation for 5 days. Groups III and IV then had recovery periods of 7 and 21 days, respectively. Spatial learning and memory was measured using the Novel Object Recognition test. The rats were euthanized with ketamine, oxidative stress was analyzed using hippocampal tissue homogenate and beta-amyloid plaques in the CA1 and CA3 regions using Congo red stain. Results: Comparing the sleep-deprived group to the sleep-recovered group, the discrimination ratio increased significantly (p < 0.0001). Sleep recovery also decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and malonaldehyde (MDA) and corticosterone (p < 0.01). Additionally, extracellular amyloid-beta expression in the CA1 and CA3 regions of the sleep recovery groups was significantly reduced (p < 0.0001 and p < 0.01). Conclusion: Recovery sleep was found to improve memory and decrease beta amyloid expression and oxidative stress in the CA1 and CA3 areas of the hippocampus.