Alzheimers disease (AD) is the most common neurodegenerative disorders in the central nervous system.Recently,environment factors have been considered a significant contributor for the development of AD.The greatly increased incidence of AD following stroke and cerebral ischemia suggests that hypoxia may be a risk factor which may facilitate AD pathogenesis by altering amyloid precursor protein (APP) processing.However,the molecular mechanism underlying the hypoxia mediated AD pathology still needs further elucidation.In present study we demonstrated that repeated hypoxia increased beta-amyloid (Aβ) deposition and neuritic plaques formation in mutant APP+PS 1 transgenic mice.Our data provide strong evidence that hypoxia facilitates beta-cleavage of APP without affecting the expression of endogenous APP.