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...

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Published in:PloS one 2022-08, Vol.17 (8), p.e0273036-e0273036
Main Authors: 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
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amino acids
Animal experimentation
Biology and Life Sciences
Brain research
Cardiovascular disease
Clustering
Computer and Information Sciences
Coumaric acid
Data integration
Diabetes mellitus
Diagnosis
Dysbacteriosis
Evaluation
Fatty acids
Feces
Genetic aspects
Health aspects
Intestinal microflora
Medicine and Health Sciences
Microbiota
Microbiota (Symbiotic organisms)
Microorganisms
Neurodegenerative diseases
Research and Analysis Methods
Statistical methods
Taxonomy
Weaning
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Summary: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.
ISSN:1932-6203
1932-6203
DOI:10.1371/journal.pone.0273036