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Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice

Alzheimer’s disease (AD) is the most common dementia in the elderly. Treatment for AD is still a difficult task in clinic. AD is associated with abnormal gut microbiota. However, little is known about the role of fecal microbiota transplantation (FMT) in AD. Here, we evaluated the efficacy of FMT fo...

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Autores principales: Sun, Jing, Xu, Jingxuan, Ling, Yi, Wang, Fangyan, Gong, Tianyu, Yang, Changwei, Ye, Shiqing, Ye, Keyue, Wei, Dianhui, Song, Ziqing, Chen, Danna, Liu, Jiaming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683152/
https://www.ncbi.nlm.nih.gov/pubmed/31383855
http://dx.doi.org/10.1038/s41398-019-0525-3
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author Sun, Jing
Xu, Jingxuan
Ling, Yi
Wang, Fangyan
Gong, Tianyu
Yang, Changwei
Ye, Shiqing
Ye, Keyue
Wei, Dianhui
Song, Ziqing
Chen, Danna
Liu, Jiaming
author_facet Sun, Jing
Xu, Jingxuan
Ling, Yi
Wang, Fangyan
Gong, Tianyu
Yang, Changwei
Ye, Shiqing
Ye, Keyue
Wei, Dianhui
Song, Ziqing
Chen, Danna
Liu, Jiaming
author_sort Sun, Jing
collection PubMed
description Alzheimer’s disease (AD) is the most common dementia in the elderly. Treatment for AD is still a difficult task in clinic. AD is associated with abnormal gut microbiota. However, little is known about the role of fecal microbiota transplantation (FMT) in AD. Here, we evaluated the efficacy of FMT for the treatment of AD. We used an APPswe/PS1dE9 transgenic (Tg) mouse model. Cognitive deficits, brain deposits of amyloid-β (Aβ) and phosphorylation of tau, synaptic plasticity as well as neuroinflammation were assessed. Gut microbiota and its metabolites short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and (1)H nuclear magnetic resonance (NMR). Our results showed that FMT treatment could improve cognitive deficits and reduce the brain deposition of amyloid-β (Aβ) in APPswe/PS1dE9 transgenic (Tg) mice. These improvements were accompanied by decreased phosphorylation of tau protein and the levels of Aβ40 and Aβ42. We observed an increases in synaptic plasticity in the Tg mice, showing that postsynaptic density protein 95 (PSD-95) and synapsin I expression were increased after FMT. We also observed the decrease of COX-2 and CD11b levels in Tg mice after FMT. We also found that FMT treatment reversed the changes of gut microbiota and SCFAs. Thus, FMT may be a potential therapeutic strategy for AD.
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spelling pubmed-66831522019-08-08 Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice Sun, Jing Xu, Jingxuan Ling, Yi Wang, Fangyan Gong, Tianyu Yang, Changwei Ye, Shiqing Ye, Keyue Wei, Dianhui Song, Ziqing Chen, Danna Liu, Jiaming Transl Psychiatry Article Alzheimer’s disease (AD) is the most common dementia in the elderly. Treatment for AD is still a difficult task in clinic. AD is associated with abnormal gut microbiota. However, little is known about the role of fecal microbiota transplantation (FMT) in AD. Here, we evaluated the efficacy of FMT for the treatment of AD. We used an APPswe/PS1dE9 transgenic (Tg) mouse model. Cognitive deficits, brain deposits of amyloid-β (Aβ) and phosphorylation of tau, synaptic plasticity as well as neuroinflammation were assessed. Gut microbiota and its metabolites short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and (1)H nuclear magnetic resonance (NMR). Our results showed that FMT treatment could improve cognitive deficits and reduce the brain deposition of amyloid-β (Aβ) in APPswe/PS1dE9 transgenic (Tg) mice. These improvements were accompanied by decreased phosphorylation of tau protein and the levels of Aβ40 and Aβ42. We observed an increases in synaptic plasticity in the Tg mice, showing that postsynaptic density protein 95 (PSD-95) and synapsin I expression were increased after FMT. We also observed the decrease of COX-2 and CD11b levels in Tg mice after FMT. We also found that FMT treatment reversed the changes of gut microbiota and SCFAs. Thus, FMT may be a potential therapeutic strategy for AD. Nature Publishing Group UK 2019-08-05 /pmc/articles/PMC6683152/ /pubmed/31383855 http://dx.doi.org/10.1038/s41398-019-0525-3 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Sun, Jing
Xu, Jingxuan
Ling, Yi
Wang, Fangyan
Gong, Tianyu
Yang, Changwei
Ye, Shiqing
Ye, Keyue
Wei, Dianhui
Song, Ziqing
Chen, Danna
Liu, Jiaming
Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title_full Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title_fullStr Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title_full_unstemmed Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title_short Fecal microbiota transplantation alleviated Alzheimer’s disease-like pathogenesis in APP/PS1 transgenic mice
title_sort fecal microbiota transplantation alleviated alzheimer’s disease-like pathogenesis in app/ps1 transgenic mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6683152/
https://www.ncbi.nlm.nih.gov/pubmed/31383855
http://dx.doi.org/10.1038/s41398-019-0525-3
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