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Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease
Sub-chronic inflammation, caused by age-related dysbiosis, primes the brain to neuroinflammation and neurodegenerative diseases. Evidence revealed that Parkinson’s disease (PD) might originate in the gut, demonstrating gastro-intestinal disturbances, as reported by PD patients long before developing...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10146107/ https://www.ncbi.nlm.nih.gov/pubmed/37110302 http://dx.doi.org/10.3390/microorganisms11040880 |
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author | Lima, Illyane S. Pêgo, Ana C. Martins, Ana C. Prada, Ana R. Barros, João Tomás Martins, Gracelino Gozzelino, Raffaella |
author_facet | Lima, Illyane S. Pêgo, Ana C. Martins, Ana C. Prada, Ana R. Barros, João Tomás Martins, Gracelino Gozzelino, Raffaella |
author_sort | Lima, Illyane S. |
collection | PubMed |
description | Sub-chronic inflammation, caused by age-related dysbiosis, primes the brain to neuroinflammation and neurodegenerative diseases. Evidence revealed that Parkinson’s disease (PD) might originate in the gut, demonstrating gastro-intestinal disturbances, as reported by PD patients long before developing motor symptoms. In this study, we conducted comparative analyses in relatively young and old mice maintained in conventional or gnotobiotic conditions. We aimed to confirm that the effects induced by age-related dysbiosis, rather than aging itself, sensitize to PD onset. This hypothesis was confirmed in germ-free (GF) mice, which proved resistant to the pharmacological induction of PD, regardless of their age. Contrary to conventional animals, old GF mice did not develop an inflammatory phenotype or an accumulation of iron in the brain, two catalysts sensitizing to disease onset. The resistance of GF mice to PD is reverted when colonized with stool collected from conventional old animals, but not if receiving bacterial content from young mice. Hence, changes in gut microbiota composition are a risk factor for PD development and can be targeted preventively by iron chelators, shown to protect the brain from pro-inflammatory intestinal priming that sensitizes to neuroinflammation and the development of severe PD. |
format | Online Article Text |
id | pubmed-10146107 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-101461072023-04-29 Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease Lima, Illyane S. Pêgo, Ana C. Martins, Ana C. Prada, Ana R. Barros, João Tomás Martins, Gracelino Gozzelino, Raffaella Microorganisms Article Sub-chronic inflammation, caused by age-related dysbiosis, primes the brain to neuroinflammation and neurodegenerative diseases. Evidence revealed that Parkinson’s disease (PD) might originate in the gut, demonstrating gastro-intestinal disturbances, as reported by PD patients long before developing motor symptoms. In this study, we conducted comparative analyses in relatively young and old mice maintained in conventional or gnotobiotic conditions. We aimed to confirm that the effects induced by age-related dysbiosis, rather than aging itself, sensitize to PD onset. This hypothesis was confirmed in germ-free (GF) mice, which proved resistant to the pharmacological induction of PD, regardless of their age. Contrary to conventional animals, old GF mice did not develop an inflammatory phenotype or an accumulation of iron in the brain, two catalysts sensitizing to disease onset. The resistance of GF mice to PD is reverted when colonized with stool collected from conventional old animals, but not if receiving bacterial content from young mice. Hence, changes in gut microbiota composition are a risk factor for PD development and can be targeted preventively by iron chelators, shown to protect the brain from pro-inflammatory intestinal priming that sensitizes to neuroinflammation and the development of severe PD. MDPI 2023-03-29 /pmc/articles/PMC10146107/ /pubmed/37110302 http://dx.doi.org/10.3390/microorganisms11040880 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Lima, Illyane S. Pêgo, Ana C. Martins, Ana C. Prada, Ana R. Barros, João Tomás Martins, Gracelino Gozzelino, Raffaella Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title | Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title_full | Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title_fullStr | Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title_full_unstemmed | Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title_short | Gut Dysbiosis: A Target for Protective Interventions against Parkinson’s Disease |
title_sort | gut dysbiosis: a target for protective interventions against parkinson’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10146107/ https://www.ncbi.nlm.nih.gov/pubmed/37110302 http://dx.doi.org/10.3390/microorganisms11040880 |
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