pISSN 1226-4512 eISSN 2093-3827

Article

home Article View

Original Article

Korean J Physiol Pharmacol 2020; 24(1): 39-46

Published online January 1, 2020 https://doi.org/10.4196/kjpp.2020.24.1.39

Copyright © The Korean Journal of Physiology & Pharmacology.

β-Sitosterol treatment attenuates cognitive deficits and prevents amyloid plaque deposition in amyloid protein precursor/presenilin 1 mice

Jian-Ya Ye1, Li Li1, Qing-Mao Hao1, Yong Qin1, and Chang-Sheng Ma2,*

1Hebei University of Chinese Medicine, Shijiazhang 050200, 2Neurobiology Laboratory, Institute of Basic Medicine, Hebei Medical University, Shijiazhang 050017, Hebei province, China

Correspondence to:*Chang-Sheng Ma
E-mail: machangsheng0311@163.com

Received: June 29, 2019; Revised: July 23, 2019; Accepted: August 5, 2019

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disorder causing dementia worldwide, and is mainly characterized by aggregated β-amyloid (Aβ). Increasing evidence has shown that plant extracts have the potential to delay AD development. The plant sterol β-Sitosterol has a potential role in inhibiting the production of platelet Aβ, suggesting that it may be useful for AD prevention. In the present study, we aimed to investigate the effect and mechanism of β-Sitosterol on deficits in learning and memory in amyloid protein precursor/presenilin 1 (APP/PS1) double transgenic mice. APP/PS1 mice were treated with β-Sitosterol for four weeks, from the age of seven months. Brain Aβ metabolism was evaluated using ELISA and Western blotting. We found that β-Sitosterol treatment can improve spatial learning and recognition memory ability, and reduce plaque load in APP/PS1 mice. β-Sitosterol treatment helped reverse dendritic spine loss in APP/PS1 mice and reversed the decreased hippocampal neuron miniature excitatory postsynaptic current frequency. Our research helps to explain and support the neuroprotective effect of β-Sitosterol, which may offer a novel pharmaceutical agent for the treatment of AD. Taken together, these findings suggest that β-Sitosterol ameliorates memory and learning impairment in APP/PS1 mice and possibly decreases Aβ deposition.

Keywords: Alzheimer disease, Amyloid-beta, β-Sitosterol, Learning and memory