Lemon essential oil ameliorates age-associated cognitive dysfunction via modulating hippocampal synaptic density and inhibiting acetylcholinesterase.

Bonan Liu,Dong Han,Bobkov Artyom,Ning Ma,Jiayuan Kou,Dehao Meng,Jiaran Xu,Xu Gao,Xiaoxi Zhou,Da Huo,Murtaza Ghulam,Fuyan Li

doi:10.18632/aging.103179

Abstract

The lemon essential oil (LEO), extracted from the fruit of lemon, has been used to treat multiple pathological diseases, such as diabetes, inflammation, cardiovascular diseases, depression and hepatobiliary dysfunction. The study was designed to study the effects of LEO on cognitive dysfunction induced by Alzheimer’s disease (AD). We used APP/PS1 double transgene (APP/PS1) AD mice in the experiment; these mice exhibit significant deficits in synaptic density and hippocampal-dependent spatial related memory. The effects of LEO on learning and memory were examined using the Morris Water Maze (MWM) test, Novel object recognition test, and correlative indicators, including a neurotransmitter (acetylcholinesterase, AChE), a nerve growth factor (brain-derived neurotrophic factor, BDNF), a postsynaptic marker (PSD95), and presynaptic markers (synapsin-1, and synaptophysin), in APP/PS1 mice. Histopathology was performed to estimate the effects of LEO on AD mice. A significantly lowered brain AChE depression in APP/PS1 and wild-type C57BL/6L (WT) mice. PSD95/ Synaptophysin, the index of synaptic density, was noticeably improved in histopathologic changes. Hence, it can be summarized that memory-enhancing activity might be associated with a reduction in the AChE levels and is elevated by BDNF, PSD95, and synaptophysin through enhancing synaptic plasticity.

Highlights

Neurodegenerative diseases of the nervous system are always related to impaired learning and memory ability, eventually inducing to cognitive disorders [1]
We investigated the effect of lemon essential oil (LEO) in the established APP/PS1 mouse model of Alzheimer’s disease (AD) and wild-type C57BL/6L (WT) mice
The most important findings of the present research were that LEO treatment partly restored hippocampal synaptic plasticity in LEO treated APP/PS1 mice

Summary

Introduction

Neurodegenerative diseases of the nervous system are always related to impaired learning and memory ability, eventually inducing to cognitive disorders [1]. AD is the leading cause of cognitive deficits and the most common neurodegenerative disease of aging [2]. It is pathologically characterized by a gradual impairment of learning and memory, accompanied by pathological characteristics such as tau protein neurofibrillary tangles and accumulation of amyloid plaques [3, 4]. Synaptic loss and impairment are the most foremost hallmarks of cognitive deficits in AD [7]. Few studies have revealed that medical compounds could treat working memory impairment and decremental LTP and have discussed the potential mechanisms [9]

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Results

Conclusion