Oligonol improves memory and cognition under an amyloid β25-35–induced Alzheimer's mouse model

Abstract Alzheimer's disease is an age-dependent progressive neurodegenerative disorder that results in impairments of memory and cognitive function. It is hypothesized that oligonol has ameliorative effects on memory impairment and reduced cognitive functions in mice with Alzheimer's disease induced by amyloid β 25-35 (A β 25-35 ) injection. The protective effect of an oligonol against A β 25-35 -induced memory impairment was investigated in an in vivo Alzheimer's mouse model. The aggregation of A β 25-35 was induced by incubation at 37°C for 3 days before injection into mice brains (5 nmol/mouse), and then oligonol was orally administered at 100 and 200 mg/kg of body weight for 2 weeks. Memory and cognition were observed in T-maze, object recognition, and Morris water maze tests. The group injected with A β 25-35 showed impairments in both recognition and memory. However, novel object recognition and new route awareness abilities were dose dependently improved by the oral administration of oligonol. In addition, the results of the Morris water maze test indicated that oligonol exerted protective activity against cognitive impairment induced by A β 25-35 . Furthermore, nitric oxide formation and lipid peroxidation were significantly elevated by A β 25-35 , whereas oligonol treatment significantly decreased nitric oxide formation and lipid peroxidation in the brain, liver, and kidneys. The present results suggest that oligonol improves A β 25-35 -induced memory deficit and cognition impairment.