Jianing Cao1, William Kwame Amakye1, Chunli Qi1, Xiaojun Liu2, Jie Ma2, Jiaoyan Ren3. 1. School of Food Science and Engineering, South China University of Technology, 381 Wu Shan Road, Guangzhou, 510641, China. 2. Beijing Scitop Bio-Tech Co. Ltd., Beijing, China. 3. School of Food Science and Engineering, South China University of Technology, 381 Wu Shan Road, Guangzhou, 510641, China. jyren@scut.edu.cn.
Abstract
PURPOSE: Studies have shown that Alzheimer's disease is associated with significant alterations in the gut microbiota. But the effect of probiotics and/or prebiotics on Alzheimer's disease still remains to be explored. The aim of this study was to determine whether Bifidobacterium Lactis Probio-M8 could alleviate Alzheimer's disease pathophysiologies in the APP/PS1 transgenic mouse model. METHODS: 4-month old APP/PS1 mice were randomly put into two groups and fed with either Probio-M8 or saline water for 45 days. Fecal samples of mice were collected at the beginning and the end of the treatment period to determine the composition of the gut microbiota via 16S ribosomal RNA sequencing technology. The number and size of Aβ plaques in the brain were quantified. In addition, Y maze, novel object recognition and nest building were employed to access cognitive function in the 8-months old APP/PS1 mice at the end of the treatment period. CONCLUSION: Our results demonstrated that Probio-M8 reduced Aβ plaque burden in the whole brain and protected against gut microbiota dysbiosis. Furthermore, Probio-M8 could alleviate cognitive impairment in the APP/PS1 mouse.
PURPOSE: Studies have shown that Alzheimer's disease is associated with significant alterations in the gut microbiota. But the effect of probiotics and/or prebiotics on Alzheimer's disease still remains to be explored. The aim of this study was to determine whether Bifidobacterium Lactis Probio-M8 could alleviate Alzheimer's disease pathophysiologies in the APP/PS1 transgenic mouse model. METHODS: 4-month old APP/PS1mice were randomly put into two groups and fed with either Probio-M8 or saline water for 45 days. Fecal samples of mice were collected at the beginning and the end of the treatment period to determine the composition of the gut microbiota via 16S ribosomal RNA sequencing technology. The number and size of Aβ plaques in the brain were quantified. In addition, Y maze, novel object recognition and nest building were employed to access cognitive function in the 8-months old APP/PS1mice at the end of the treatment period. CONCLUSION: Our results demonstrated that Probio-M8 reduced Aβ plaque burden in the whole brain and protected against gut microbiota dysbiosis. Furthermore, Probio-M8 could alleviate cognitive impairment in the APP/PS1mouse.
Entities:
Keywords:
APP/PS1 mouse; Aβ; Bifidobacterium Lactis; Gut microbiota; Probio-M8
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