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“Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration

Wheat is a most favored staple food worldwide and its major protein is gluten. It is involved in several gluten dependent diseases and lately was suggested to play a role in non-celiac autoimmune diseases. Its involvement in neurodegenerative conditions was recently suggested but no cause-and-effect...

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Autores principales: Lerner, Aaron, Benzvi, Carina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065505/
https://www.ncbi.nlm.nih.gov/pubmed/33808124
http://dx.doi.org/10.3390/cells10040756
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author Lerner, Aaron
Benzvi, Carina
author_facet Lerner, Aaron
Benzvi, Carina
author_sort Lerner, Aaron
collection PubMed
description Wheat is a most favored staple food worldwide and its major protein is gluten. It is involved in several gluten dependent diseases and lately was suggested to play a role in non-celiac autoimmune diseases. Its involvement in neurodegenerative conditions was recently suggested but no cause-and-effect relationship were established. The present narrative review expands on various aspects of the gluten-gut-brain axes events, mechanisms and pathways that connect wheat and gluten consumption to neurodegenerative disease. Gluten induced dysbiosis, increased intestinal permeabillity, enteric and systemic side effects, cross-reactive antibodies, and the sequence of homologies between brain antigens and gluten are highlighted. This combination may suggest molecular mimicry, alluding to some autoimmune aspects between gluten and neurodegenerative disease. The proverb of Hippocrates coined in 400 BC, “let food be thy medicine,” is critically discussed in the frame of gluten and potential neurodegeneration evolvement.
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spelling pubmed-80655052021-04-25 “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration Lerner, Aaron Benzvi, Carina Cells Review Wheat is a most favored staple food worldwide and its major protein is gluten. It is involved in several gluten dependent diseases and lately was suggested to play a role in non-celiac autoimmune diseases. Its involvement in neurodegenerative conditions was recently suggested but no cause-and-effect relationship were established. The present narrative review expands on various aspects of the gluten-gut-brain axes events, mechanisms and pathways that connect wheat and gluten consumption to neurodegenerative disease. Gluten induced dysbiosis, increased intestinal permeabillity, enteric and systemic side effects, cross-reactive antibodies, and the sequence of homologies between brain antigens and gluten are highlighted. This combination may suggest molecular mimicry, alluding to some autoimmune aspects between gluten and neurodegenerative disease. The proverb of Hippocrates coined in 400 BC, “let food be thy medicine,” is critically discussed in the frame of gluten and potential neurodegeneration evolvement. MDPI 2021-03-30 /pmc/articles/PMC8065505/ /pubmed/33808124 http://dx.doi.org/10.3390/cells10040756 Text en © 2021 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 (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Review
Lerner, Aaron
Benzvi, Carina
“Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title_full “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title_fullStr “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title_full_unstemmed “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title_short “Let Food Be Thy Medicine”: Gluten and Potential Role in Neurodegeneration
title_sort “let food be thy medicine”: gluten and potential role in neurodegeneration
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8065505/
https://www.ncbi.nlm.nih.gov/pubmed/33808124
http://dx.doi.org/10.3390/cells10040756
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