Obstructive sleep apnea syndrome (OSAS) is characterized by chronic nocturnal intermittent hypoxia and sleep fragmentations.Neurocognitive dysfunction, a significant and extraordinary complication of OSAS, seriously influences the patients work, family and social life and reduces quality of life.Cognitive impairment in OSAS could be involved in a series of cognitive domain, such as attention/vigilance, memory, global cognitive function, executive function.More importantly, evidence, which accumulated in recentyears, has demonstrated that oxidative stress (OS) that results from chronic recurrent hypoxia and reoxygenation, an extraordinary characteristic of OSAS, is one of important mechanisms leading to neurocognitive dysfunction.Repetitive episodes of obstruction of the upper airway induces chronic intermittent hypoxia(CIH), then causes dysfunction of mitochondria, endoplasmic reticulum,energy metabolism and endothelium , activation of NADPH oxidase, xanthine oxidase and a series of inflammation reaction,consequently contributes to overproduction of reactive oxygen species(ROS) and imbalance of oxidation-antioxidation, that is state of oxidative stress, which produces protein, lipid and DNA peroxidation damage.However, cerebral neural cells, especially in the region of hippocampus and cerebral cortex, are susceptible to hypoxemia.CIH-induced OS could lead to the necrosis and apoptosis of nerve cell, which results in neurocognitive dysfunction of OSAS gradually, presenting near-term declined attention and vigilance and long-term degeneration of memory, executive function.In addition to continue positive airway pressure(CPAP) treatment, animal experiments of OSAS demonstrate that administration of antioxidant, erythropoietin, growth hormone, growth hormone releasing hormone (GHRH) agonist JI-34 and telmisartan might provide an available measure to protect IHvulnerable brain regions from OSAS-associated neuronal damage and associated neurocognitive dysfunction.However, neither has definite evidence verified the relationship between oxidative stress and neurocognitive dysfunction in OSAS patients, nor have available clinical trials confirmed the effectiveness of above medicine so far.Moreover, specific upstream or downstream molecular mechanisms involved in the OS-induced cognitive impairment have still been not clear.