Alzheimers disease (AD) is the most prevalent form of neurodegenerations associated with aging in the human population. This disease is characterized by the extracellular deposition of beta-amyloid (A ${eta}$) peptide in cerebral plaques. The A ${eta}$ peptide is derived from the ${eta}$-amyloid precursor protein ( ${eta}$APP). Photolytic processing of ${eta}$APP by ${eta}$-secretase(beta-site APP-cleaving enzyme, BASE) and ${gamma}$-secretase generates the A ${eta}$ peptide. Several lines of evidence support that A ${eta}$-induced neuronal cell death is major mechanisms of development of AD. Accordingly, the ${eta}$-and ${gamma}$-secretase have been implicated to be excellent targets for the treatment of AD. We previously found that sesaminol glucosides have improving effect on memory functions through anti-oxidative mechanism. In this study, to elucidate possible other mechanism (inhibition of ${eta}$-and ${gamma}$-secretase) of sesaminol glucosides, we examined the improving effect of sesaminol glucosides in the scopolamine (1 mg/kg/mouse)-induced memory dysfunction using water maze test in the mice. Sesaminol glucosides (3.75, 7.5 mg/kg/6ml/day p.o., for 3 weeks) reversed the latency time, distance and velocity by scopolamine in dose dependent manner. Next, ${eta}$-and ${gamma}$-secretase activities were determined in different regions of brain. Sesaminol glucosides dose-dependently attenuated scopolamine-induced ${eta}$-secretase activities in cortex and hippocampous and ${gamma}$-secretase in cortex. This study therefore suggests that sesaminol glucosides may be a useful agent for prevention of the development or progression of AD, and its inhibitory effect on secretase may play a role in the improving action of sesaminol glucosides on memory function.