P2-044: the effect of standardized extract of asian herb im01 on conditioned fear memory deficit of 3xtg-ad mice

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by extracellular amyloid plaques and intracellular neurofibrillary tangles. Inflammatory changes are observed in AD brain, caused by microglia activation. Activation of microglial lead to release of pro-inflammatory cytokine, free radicals and nitric oxide (NO), which can induces neuronal damage and progression in AD pathogenesis. Until now there is no effective pharmacotherapeutic agent for preventing or treating AD. IM01 is extracted from one herb commonly grown in south Asia. It has been reported to have neuroprotective effective in treating memory impairment induced by intracerebroventricular injection of amyloid-β, also in transient global ischemia (T2VO). In this study, we aims to investigate the effect of IM01 on treating deficit of conditioned fear memory retrieval in triple-transgenic Alzheimer's disease (3xTg-AD) model mice. The 5-6-month-old, age-matching, 3xTg-AD mice and non-transgenic mice on 129/C57BL6 background were used in this study. Mice were divided into 6 groups: non-transgenic control untreated (non-Tg-untreated), 3xTg untreated, 3xTg-Sham, 3xTg treated with IM01 of 10, 30 and 100 mg/kg. IM01 was orally administered to mice twice a day for 30 consecutive days. After treatment all mice were tested with performance of trace fear conditioning. Our preliminary results showed that 3xTg untreated group exhibited abnormal learning ability. The 3xTg untreated group showed significant decrease in freezing behavior to cue, however, the abnormal phenotype was reversed after treated with IM01. Present results revealed that IM01 treatment may improve retrieval of cued fear memory in 3xTg-AD model mice. Further studies are required to investigate the molecular mechanism of IM01 effect on memory performance. The IM01 may become a promising natural product that provides alternative treatment for Alzheimer's disease.