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Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease

Several studies investigating the pathogenesis of Alzheimer’s disease have identified various interdependent constituents contributing to the exacerbation of the disease, including Aβ plaque formation, tau protein hyperphosphorylation, neurofibrillary tangle accumulation, glial inflammation, and the...

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Autores principales: Lee, Daniel, Lee, Virginia M-Y., Hur, Seong Kwon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9672822/
https://www.ncbi.nlm.nih.gov/pubmed/36408394
http://dx.doi.org/10.3389/fnins.2022.1042865
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author Lee, Daniel
Lee, Virginia M-Y.
Hur, Seong Kwon
author_facet Lee, Daniel
Lee, Virginia M-Y.
Hur, Seong Kwon
author_sort Lee, Daniel
collection PubMed
description Several studies investigating the pathogenesis of Alzheimer’s disease have identified various interdependent constituents contributing to the exacerbation of the disease, including Aβ plaque formation, tau protein hyperphosphorylation, neurofibrillary tangle accumulation, glial inflammation, and the eventual loss of proper neural plasticity. Recently, using various models and human patients, another key factor has been established as an influential determinant in brain homeostasis: the gut–brain axis. The implications of a rapidly aging population and the absence of a definitive cure for Alzheimer’s disease have prompted a search for non-pharmaceutical tools, of which gut-modulatory therapies targeting the gut–brain axis have shown promise. Yet multiple recent studies examining changes in human gut flora in response to various probiotics and environmental factors are limited and difficult to generalize; whether the state of the gut microbiota in Alzheimer’s disease is a cause of the disease, a result of the disease, or both through numerous feedback loops in the gut–brain axis, remains unclear. However, preliminary findings of longitudinal studies conducted over the past decades have highlighted dietary interventions, especially Mediterranean diets, as preventative measures for Alzheimer’s disease by reversing neuroinflammation, modifying the intestinal and blood–brain barrier (BBB), and addressing gut dysbiosis. Conversely, the consumption of Western diets intensifies the progression of Alzheimer’s disease through genetic alterations, impaired barrier function, and chronic inflammation. This review aims to support the growing body of experimental and clinical data highlighting specific probiotic strains and particular dietary components in preventing Alzheimer’s disease via the gut–brain axis.
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spelling pubmed-96728222022-11-19 Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease Lee, Daniel Lee, Virginia M-Y. Hur, Seong Kwon Front Neurosci Neuroscience Several studies investigating the pathogenesis of Alzheimer’s disease have identified various interdependent constituents contributing to the exacerbation of the disease, including Aβ plaque formation, tau protein hyperphosphorylation, neurofibrillary tangle accumulation, glial inflammation, and the eventual loss of proper neural plasticity. Recently, using various models and human patients, another key factor has been established as an influential determinant in brain homeostasis: the gut–brain axis. The implications of a rapidly aging population and the absence of a definitive cure for Alzheimer’s disease have prompted a search for non-pharmaceutical tools, of which gut-modulatory therapies targeting the gut–brain axis have shown promise. Yet multiple recent studies examining changes in human gut flora in response to various probiotics and environmental factors are limited and difficult to generalize; whether the state of the gut microbiota in Alzheimer’s disease is a cause of the disease, a result of the disease, or both through numerous feedback loops in the gut–brain axis, remains unclear. However, preliminary findings of longitudinal studies conducted over the past decades have highlighted dietary interventions, especially Mediterranean diets, as preventative measures for Alzheimer’s disease by reversing neuroinflammation, modifying the intestinal and blood–brain barrier (BBB), and addressing gut dysbiosis. Conversely, the consumption of Western diets intensifies the progression of Alzheimer’s disease through genetic alterations, impaired barrier function, and chronic inflammation. This review aims to support the growing body of experimental and clinical data highlighting specific probiotic strains and particular dietary components in preventing Alzheimer’s disease via the gut–brain axis. Frontiers Media S.A. 2022-11-04 /pmc/articles/PMC9672822/ /pubmed/36408394 http://dx.doi.org/10.3389/fnins.2022.1042865 Text en Copyright © 2022 Lee, Lee and Hur. 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
Lee, Daniel
Lee, Virginia M-Y.
Hur, Seong Kwon
Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title_full Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title_fullStr Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title_full_unstemmed Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title_short Manipulation of the diet–microbiota–brain axis in Alzheimer’s disease
title_sort manipulation of the diet–microbiota–brain axis in alzheimer’s disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9672822/
https://www.ncbi.nlm.nih.gov/pubmed/36408394
http://dx.doi.org/10.3389/fnins.2022.1042865
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