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Introduction: Sleep has been found to influence both acquisition and consolidation of memory; therefore, sleep deprivation is often linked to multiple anomalies in cognitive paradigms giving rise cognitive dysfunctions. Objective: The present study has been designed with an aim to decipher plausible mechanistic interplays involved in the induction of cognitive dysfunction as a direct consequence of sleep deprivation. Methods: Male laca mice were sleep deprived for 24-hours using grid suspended over water method on alternate days extended over the total protocol duration of 21 days. Various neurobehavioral memory evaluating parameters followed by biochemical, acetylcholinesterase (AChE) activity, mitochondrial respiratory enzyme complex activities (I-IV) and histopathological examinations of the mice brain were monitored. Results: Sleep deprivation of 24-hours on alternate days for 21 days significantly impaired cognitive performance in both memory evaluating paradigms (Morris water maze test and elevated plus maze test) as compared to naïve animals. Additionally animals subjected to sleep deprivation also demonstrated conditions of elevated oxidative stress, impaired mitochondrial enzyme complex activities, increased aceytlcholineestaerase activity, as well as histopathological alterations pertaining to hippocampal and thalamo-cortical regions of mice brain as compared to naïve animals. However, chronic piracetam (100 mg/kg) treatment showed significant protective effect against sleep deprivation induced cognitive dysfunction, oxidative damage, mitochondrial respiratory enzyme complex insuffeciencies, increased acetylcholinesterase activity as well as neuromorphological alterations. Conclusion: The present study suggests mechanistic interplay between oxidative stresses; mitochondrial impairment as well as acetylcholineesterase activity may influence hippocampal and cortical neuronal survival and thus lead to precipitation of sleep deprivation induced cognitive deficits.