Biol. Pharm. Bull. 29(1) 71—74 (2006)

characterized by irreversible, progressive loss of memory followed by complete dementia. Cognitive impairment in AD is caused mainly by death of cholinergic neurons in basal forebrain area, though other neurotransmitter systems could well be involved. A deficit of acetylcholine (ACh) in an AD brain is well known. At the same time, extent of dementia correlates well with the extent of neuronal death caused by excess of glutamate, the most prevalent excitatory neurotransmitter in the brain. We previously reported that ten phenylethanoid glycosides including acteoside (Fig. 1) isolated from the leaves and twigs of Callicarpa dichotoma (Verbenaceae) significantly attenuated glutamate-induced neurotoxicity. In the present study, we tried to examine whether the major constituent, acteoside mitigated scopolamine-induced memory impairment in mice. Acteoside ( Verbascoside, Fig. 1) is a phenylethanoid glycoside distributed in C. dichotoma and other medicinal plants. Many studies have reported that acteoside shows anti-oxidative, anti-inflammatory, antinephritic and anti-hepatotoxic activities. It contains a hydroxyphenylethyl and a caffeoyl moiety which are wellknown antioxidants. To assess the efficacy of the acteoside, mice were treated with acteoside and then scopolamine was used to induce memory impairment. The degree of impairment was gauged using both the passive avoidance and the Morris water maze tests with or without treatment with acteoside.