Cognitive-Enhancing Effect of Aronia melanocarpa Extract against Memory Impairment Induced by Scopolamine in Mice.

Hyeon Yong Lee,Choong Je Ma,Youn Sik Jung,Nam Young Kim,Myong Ki Kim,Jin Bae Weon

doi:10.1155/2016/6145926

Abstract

Aronia melanocarpa (A. melanocarpa) berries are a fruit with a marked antioxidant effect. The objective of this study was to confirm the effect of A. melanocarpa berries extract against scopolamine-induced memory impairment in mice using the Morris water maze and passive avoidance test. Moreover, we determined a possible mechanism of the cognitive-enhancing effect involving AChE activity and BDNF and p-CREB expression in the hippocampus of mice. A. melanocarpa berries extract attenuated the learning and memory impairment induced by scopolamine in the Morris water maze (79.3 ± 0.8 s of 200 mg/kg and 64.4 ± 10.7 s of 400 mg/kg on day 4) and passive avoidance tests (46.0 ± 41.1 s of 200 mg/kg and 25.6 ± 18.7 s of 400 mg/kg). A. melanocarpa berries extract reduced the acetylcholinesterase level in the hippocampus of scopolamine-injected mice and increased BDNF and p-CREB expression in the hippocampus. The major compound, cyanidin-3-O-galactoside, also reversed memory impairment. These results showed that A. melanocarpa berries extract improved memory impairment by inhibiting AChE and increasing BDNF and p-CREB expression, and cyanidin-3-O-galactoside may be responsible for the effect of A. melanocarpa berries extract.

Highlights

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that results in memory loss and cognitive dysfunction and is the most common cause of dementia [1]
We revealed the effect of A. melanocarpa berries extract and cyanidin-3-O-galactoside on scopolamine-induced memory deficits in the Morris water maze and passive avoidance tests
The effect of A. melanocarpa berries extract (200 and 400 mg/kg) on scopolamine-induced spatial memory impairment was evaluated by means of the Morris water maze test (Figure 2(a))

Summary

Introduction

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that results in memory loss and cognitive dysfunction and is the most common cause of dementia [1]. The symptoms of AD are generally cognitive and memory loss. A characteristic pathogenesis, extracellular deposition of amyloid plaque deposits (Aβ), neurofibrillary tangles (NFT), cholinergic deficiency, and neuronal cell death, is seen in the brains of AD patients [2,3,4]. Acetylcholine (ACh) is a primary neurotransmitter in interneurons of the central nervous system (CNS) and ACh dysfunction is responsible for memory and cognitive function impairment in the CNS by cholinergic system deficiency [5]. Acetylcholinesterase (AChE) hydrolyses ACh to choline and acetic acid. High level of AChE can be not good for memory function

Objectives

Methods

Results

Conclusion