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A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease
The key role played by host-microbiota interactions on human health, disease onset and progression, and on host response to treatments has increasingly emerged in the latest decades. Indeed, dysbiosis has been associated to several human diseases such as obesity, diabetes, cancer and also neurodegen...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9401139/ https://www.ncbi.nlm.nih.gov/pubmed/36001607 http://dx.doi.org/10.1371/journal.pone.0273036 |
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author | Favero, Francesco Barberis, Elettra Gagliardi, Mara Espinoza, Stefano Contu, Liliana Gustincich, Stefano Boccafoschi, Francesca Borsotti, Chiara Lim, Dmitry Rubino, Vito Mignone, Flavio Pasolli, Edoardo Manfredi, Marcello Zucchelli, Silvia Corà, Davide Corazzari, Marco |
author_facet | Favero, Francesco Barberis, Elettra Gagliardi, Mara Espinoza, Stefano Contu, Liliana Gustincich, Stefano Boccafoschi, Francesca Borsotti, Chiara Lim, Dmitry Rubino, Vito Mignone, Flavio Pasolli, Edoardo Manfredi, Marcello Zucchelli, Silvia Corà, Davide Corazzari, Marco |
author_sort | Favero, Francesco |
collection | PubMed |
description | The key role played by host-microbiota interactions on human health, disease onset and progression, and on host response to treatments has increasingly emerged in the latest decades. Indeed, dysbiosis has been associated to several human diseases such as obesity, diabetes, cancer and also neurodegenerative disease, such as Parkinson, Huntington and Alzheimer’s disease (AD), although whether causative, consequence or merely an epiphenomenon is still under investigation. In the present study, we performed a metabologenomic analysis of stool samples from a mouse model of AD, the 3xTgAD. We found a significant change in the microbiota of AD mice compared to WT, with a longitudinal divergence of the F/B ratio, a parameter suggesting a gut dysbiosis. Moreover, AD mice showed a significant decrease of some amino acids, while data integration revealed a dysregulated production of desaminotyrosine (DAT) and dihydro-3-coumaric acid. Collectively, our data show a dysregulated gut microbiota associated to the onset and progression of AD, also indicating that a dysbiosis can occur prior to significant clinical signs, evidenced by early SCFA alterations, compatible with gut inflammation. |
format | Online Article Text |
id | pubmed-9401139 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-94011392022-08-25 A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease Favero, Francesco Barberis, Elettra Gagliardi, Mara Espinoza, Stefano Contu, Liliana Gustincich, Stefano Boccafoschi, Francesca Borsotti, Chiara Lim, Dmitry Rubino, Vito Mignone, Flavio Pasolli, Edoardo Manfredi, Marcello Zucchelli, Silvia Corà, Davide Corazzari, Marco PLoS One Research Article The key role played by host-microbiota interactions on human health, disease onset and progression, and on host response to treatments has increasingly emerged in the latest decades. Indeed, dysbiosis has been associated to several human diseases such as obesity, diabetes, cancer and also neurodegenerative disease, such as Parkinson, Huntington and Alzheimer’s disease (AD), although whether causative, consequence or merely an epiphenomenon is still under investigation. In the present study, we performed a metabologenomic analysis of stool samples from a mouse model of AD, the 3xTgAD. We found a significant change in the microbiota of AD mice compared to WT, with a longitudinal divergence of the F/B ratio, a parameter suggesting a gut dysbiosis. Moreover, AD mice showed a significant decrease of some amino acids, while data integration revealed a dysregulated production of desaminotyrosine (DAT) and dihydro-3-coumaric acid. Collectively, our data show a dysregulated gut microbiota associated to the onset and progression of AD, also indicating that a dysbiosis can occur prior to significant clinical signs, evidenced by early SCFA alterations, compatible with gut inflammation. Public Library of Science 2022-08-24 /pmc/articles/PMC9401139/ /pubmed/36001607 http://dx.doi.org/10.1371/journal.pone.0273036 Text en © 2022 Favero et al https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Favero, Francesco Barberis, Elettra Gagliardi, Mara Espinoza, Stefano Contu, Liliana Gustincich, Stefano Boccafoschi, Francesca Borsotti, Chiara Lim, Dmitry Rubino, Vito Mignone, Flavio Pasolli, Edoardo Manfredi, Marcello Zucchelli, Silvia Corà, Davide Corazzari, Marco A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title | A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title_full | A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title_fullStr | A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title_full_unstemmed | A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title_short | A Metabologenomic approach reveals alterations in the gut microbiota of a mouse model of Alzheimer’s disease |
title_sort | metabologenomic approach reveals alterations in the gut microbiota of a mouse model of alzheimer’s disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9401139/ https://www.ncbi.nlm.nih.gov/pubmed/36001607 http://dx.doi.org/10.1371/journal.pone.0273036 |
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