Dehydroeffusol Rescues Amyloid β_25-35-Induced Spatial Working Memory Deficit

Amyloid β (Aβ) peptides produced from the amyloid precursor protein, a transmembrane protein, are neurotoxic and blocking the neurotoxicity may lead to prevention of Alzheimer's disease (AD). Here we tested whether Aβ_25-35-induced cognitive decline is rescued by treatment with dehydroeffusol, a phenanthrene isolated from Chinese medicine Juncus effusus. Dehydroeffusol (5 ~ 15 mg/kg body weight) was orally administered to mice for 6 days and Aβ_25-35 (2 mM) was injected at the rate of 1 μl/min for 3 min into the lateral ventricle. Y-maze test was performed after dehydroeffusol administration for 12 days. Aβ_25-35 impaired learning and memory in the test, while the impairment was dose-dependently rescued by dehydroeffusol administration. The present study indicates that treatment with dehydroeffusol is effective for rescuing Aβ_25-35-induced cognitive decline.