Vaccinium uliginosum L. Improves Amyloid β Protein-Induced Learning and Memory Impairment in Alzheimer’s Disease in Mice

The present study investigated the effects of Vaccinium uliginosum L. (bilberry) on the learning and memory impairments induced by amyloid-β protein (AβP) 1-42. ICR Swiss mice were divided into 4 groups: the control (Aβ40-1A), control with 5% bilberry group (Aβ40-1B), amyloid β protein 1-42 treated group (Aβ1-42A), and Aβ1-42 with 5% bilberry group (Aβ1-42B). The control was treated with amyloid β-protein 40-1 for placebo effect, and Alzheimer’s disease (AD) group was treated with amyloid β-protein 1-42. Amyloid β-protein 1-42 was intracerebroventricular (ICV) micro injected into the hippocampus in 35% acetonitrile and 0.1% trifluoroacetic acid. Although bilberry added groups tended to decrease the finding time of hidden platform, no statistical significance was found. On the other hand, escape latencies of AβP injected mice were extended compared to that of Aβ40-1. In the Probe test, bilberry added Aβ1-42B group showed a significant (P<0.05) increase of probe crossing frequency compared to Aβ1-42A. Administration of amyloid protein (Aβ1-42) decreased working memory compared to Aβ40-1 control group. In passive avoidance test, bilberry significantly (P<0.05) increased the time of staying in the lighted area compared to AD control. The results suggest that bilberry may help to improve memory and learning capability in chemically induced Alzheimer’s disease in experimental animal models.