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The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion
Alzheimer's disease (AD) is a primary, progressive, neurodegenerative disorder. Many risk factors for the development of AD have been investigated, including nutrition. Although it has been proven that nutrition plays a role in AD, the precise mechanisms through which nutrition exerts its influ...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417586/ https://www.ncbi.nlm.nih.gov/pubmed/34489620 http://dx.doi.org/10.3389/fnins.2021.677777 |
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author | Bello-Corral, Laura Sánchez-Valdeón, Leticia Casado-Verdejo, Inés Seco-Calvo, Jesús Ángel Antonio Fernández-Fernández, Jesús Nélida Fernández-Martínez, María |
author_facet | Bello-Corral, Laura Sánchez-Valdeón, Leticia Casado-Verdejo, Inés Seco-Calvo, Jesús Ángel Antonio Fernández-Fernández, Jesús Nélida Fernández-Martínez, María |
author_sort | Bello-Corral, Laura |
collection | PubMed |
description | Alzheimer's disease (AD) is a primary, progressive, neurodegenerative disorder. Many risk factors for the development of AD have been investigated, including nutrition. Although it has been proven that nutrition plays a role in AD, the precise mechanisms through which nutrition exerts its influence remain undefined. The object of this study is to address this issue by elucidating some of the mechanisms through which nutrition interacts with AD. This work is a qualitative systematic bibliographic review of the current literature searchable on various available databases, including PubMed, Web of Science, and Google Scholar. Our evidence comprises 31 articles selected after a systematic search process. Patients suffering with AD present a characteristic microbiome that promotes changes in microglia generating a proinflammatory state. Many similarities exist between AD and prion diseases, both in terms of symptoms and in the molecular mechanisms of pathogenesis. Changes in the composition of the gut microbiome due to dietary habits could be one of the environmental factors affecting the development of AD; however, this is probably not the only factor. Similarly, the mechanism for self-propagation of beta-amyloid seen in AD is similar to that seen in prions. |
format | Online Article Text |
id | pubmed-8417586 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-84175862021-09-05 The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion Bello-Corral, Laura Sánchez-Valdeón, Leticia Casado-Verdejo, Inés Seco-Calvo, Jesús Ángel Antonio Fernández-Fernández, Jesús Nélida Fernández-Martínez, María Front Neurosci Neuroscience Alzheimer's disease (AD) is a primary, progressive, neurodegenerative disorder. Many risk factors for the development of AD have been investigated, including nutrition. Although it has been proven that nutrition plays a role in AD, the precise mechanisms through which nutrition exerts its influence remain undefined. The object of this study is to address this issue by elucidating some of the mechanisms through which nutrition interacts with AD. This work is a qualitative systematic bibliographic review of the current literature searchable on various available databases, including PubMed, Web of Science, and Google Scholar. Our evidence comprises 31 articles selected after a systematic search process. Patients suffering with AD present a characteristic microbiome that promotes changes in microglia generating a proinflammatory state. Many similarities exist between AD and prion diseases, both in terms of symptoms and in the molecular mechanisms of pathogenesis. Changes in the composition of the gut microbiome due to dietary habits could be one of the environmental factors affecting the development of AD; however, this is probably not the only factor. Similarly, the mechanism for self-propagation of beta-amyloid seen in AD is similar to that seen in prions. Frontiers Media S.A. 2021-08-20 /pmc/articles/PMC8417586/ /pubmed/34489620 http://dx.doi.org/10.3389/fnins.2021.677777 Text en Copyright © 2021 Bello-Corral, Sánchez-Valdeón, Casado-Verdejo, Seco-Calvo, Antonio Fernández-Fernández and Nélida Fernández-Martínez. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Bello-Corral, Laura Sánchez-Valdeón, Leticia Casado-Verdejo, Inés Seco-Calvo, Jesús Ángel Antonio Fernández-Fernández, Jesús Nélida Fernández-Martínez, María The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title | The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title_full | The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title_fullStr | The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title_full_unstemmed | The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title_short | The Influence of Nutrition in Alzheimer's Disease: Neuroinflammation and the Microbiome vs. Transmissible Prion |
title_sort | influence of nutrition in alzheimer's disease: neuroinflammation and the microbiome vs. transmissible prion |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417586/ https://www.ncbi.nlm.nih.gov/pubmed/34489620 http://dx.doi.org/10.3389/fnins.2021.677777 |
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