Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment. Codonopsis lanceolata (C. lanceolata) has been employed clinically for lung inflammatory diseases such as asthma, tonsillitis, and pharyngitis. The present study was undertaken to evaluate the effect of fermented C. lanceolata (300, 500, and 800 mg/kg) on learning and memory impairment induced by scopolamine by using the Morris water maze and passive avoidance tests. To elucidate possible mechanism of cognitive-enhancing activity, we measured acetylcholinesterase (AchE) activity, brain-derived neurotrophic factor (BDNF), and cyclic AMP response element-binding protein (CREB) expression in the brain of mice. Administration of fermented C. lanceolata (800 mg/kg) led to reduced scopolamine-induced memory impairment in the Morris water maze and passive avoidance tests. Accordingly, the administration of fermented C. lanceolata inhibited AchE activity. Interestingly, the level of CREB phosphorylation and BDNF expression in hippocampal tissue of scopolamine-treated mice was significantly increased by the administration of fermented C. lanceolata. These results indicate that fermented C. lanceolata can ameliorate scopolamine-induced memory deficits in mouse and may be an alternative agent for the treatment of AD.

Highlights

  • Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that results in impaired memory and cognition and is the most common cause of dementia among older people [1, 2]

  • After modifying the steam and fermentation process for the mass production of steamed and fermented C. lanceolata, we investigated the effect of newly processed steamed and fermented C. lanceolata extract on scopolamine-induced spatial memory impairment by using the Morris water maze test (Figure 1)

  • In the Morris water maze test, significant effects were observed for the fermented C. lanceolata group for treatment [F(6, 98) = 2.21, P < 0.001], for days [F(3, 98) = 2.87, P < 0.001], and for the interaction between treatment and day [F(18, 98) = 1.82, P = 0.95]

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Summary

Introduction

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that results in impaired memory and cognition and is the most common cause of dementia among older people [1, 2]. There are multiple causes of AD and some causes have yet to be discovered. The pathogenesis of AD is defined by the presence of senile plaques, neurofibrillary tangles, and several biochemical factors such as inflammation and oxidative stress. Plaques are formed by the accumulation of β-amyloid, and inflammation around plaques in the brain can lead to cell death. Neurofibrillary tangles consist of the protein tau, a microtubule-associated protein. The presence of neurofibrillary tangles, together with the accumulation of β-amyloid, interferes with normal cellular functioning

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