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Ameliorative effect of vanillin on scopolamine-induced dementia-like cognitive impairment in a mouse model

东莨菪碱 认知障碍 痴呆 香兰素 医学 神经科学 认知 药理学 心理学 内科学 化学 疾病 食品科学
作者
Abhinav Anand,Navneet Khurana,Nemat Ali,Abdullah F. Alasmari,Metab Alharbi,Mohammad Waseem,Neha Sharma
出处
期刊:Frontiers in Neuroscience [Frontiers Media]
卷期号:16: 1005972-1005972 被引量:12
标识
DOI:10.3389/fnins.2022.1005972
摘要

Background Alzheimer’s disease (AD) is the most common form of dementia, which is among the top five causes of death in the United States. It is a neurodegenerative disorder that causes permanent loss of memory and cognition. The current pharmacotherapy for AD is based on providing symptomatic relief only and has many side effects. There is a need for a safer, disease-modifying drug for the treatment of AD. Experimental approach The PASS online software was used to screen phytoconstituents based on their predicted effects on various AD-related targets. Vanillin was selected as the compound of interest, as it has not been researched elaborately on any animal model of AD. The acetylcholinesterase inhibitory activity of vanillin was established in vitro . Thereafter, ameliorative effect of vanillin was evaluated using the exteroceptive memory model in scopolamine-induced cognitive impairment mice model. Results Vanillin showed an acetylcholinesterase inhibitory activity in vitro , and the IC 50 value was calculated to be 0.033 mM. Vanillin significantly reversed the memory and behavioral deficits caused by scopolamine as demonstrated by significant improvement in memory in negative reinforcement, elevated plus maze, and spatial learning paradigms. Vanillin also proved to have a nootropic effect. Also, vanillin proved to have significantly better antioxidant and acetylcholinesterase inhibitory effects in vivo than donepezil hydrochloride. The potential anti-AD activity of vanillin was also confirmed by the reduction in IL-6 levels and TNF-α levels. Conclusion Our results suggest that vanillin is a safe and effective natural drug candidate having a great potential for the treatment of AD. However, more research is required to evaluate its effect on A beta plaques and Tau neurofibrillary tangles in vivo .
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