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The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition

Aging is inevitable and it is one of the major contributors to cognitive decline. However, the mechanisms underlying age-related cognitive decline are still the object of extensive research. At the biological level, it is unknown how the aging brain is subjected to progressive oxidative stress and n...

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Autores principales: Kaliszewska, Aleksandra, Allison, Joseph, Martini, Matteo, Arias, Natalia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8036520/
https://www.ncbi.nlm.nih.gov/pubmed/33808221
http://dx.doi.org/10.3390/ijms22073574
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author Kaliszewska, Aleksandra
Allison, Joseph
Martini, Matteo
Arias, Natalia
author_facet Kaliszewska, Aleksandra
Allison, Joseph
Martini, Matteo
Arias, Natalia
author_sort Kaliszewska, Aleksandra
collection PubMed
description Aging is inevitable and it is one of the major contributors to cognitive decline. However, the mechanisms underlying age-related cognitive decline are still the object of extensive research. At the biological level, it is unknown how the aging brain is subjected to progressive oxidative stress and neuroinflammation which determine, among others, mitochondrial dysfunction. The link between mitochondrial dysfunction and cognitive impairment is becoming ever more clear by the presence of significant neurological disturbances in human mitochondrial diseases. Possibly, the most important lifestyle factor determining mitochondrial functioning is nutrition. Therefore, with the present work, we review the latest findings disclosing a link between nutrition, mitochondrial functioning and cognition, and pave new ways to counteract cognitive decline in late adulthood through diet.
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spelling pubmed-80365202021-04-12 The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition Kaliszewska, Aleksandra Allison, Joseph Martini, Matteo Arias, Natalia Int J Mol Sci Review Aging is inevitable and it is one of the major contributors to cognitive decline. However, the mechanisms underlying age-related cognitive decline are still the object of extensive research. At the biological level, it is unknown how the aging brain is subjected to progressive oxidative stress and neuroinflammation which determine, among others, mitochondrial dysfunction. The link between mitochondrial dysfunction and cognitive impairment is becoming ever more clear by the presence of significant neurological disturbances in human mitochondrial diseases. Possibly, the most important lifestyle factor determining mitochondrial functioning is nutrition. Therefore, with the present work, we review the latest findings disclosing a link between nutrition, mitochondrial functioning and cognition, and pave new ways to counteract cognitive decline in late adulthood through diet. MDPI 2021-03-30 /pmc/articles/PMC8036520/ /pubmed/33808221 http://dx.doi.org/10.3390/ijms22073574 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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kaliszewska, Aleksandra
Allison, Joseph
Martini, Matteo
Arias, Natalia
The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title_full The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title_fullStr The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title_full_unstemmed The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title_short The Interaction of Diet and Mitochondrial Dysfunction in Aging and Cognition
title_sort interaction of diet and mitochondrial dysfunction in aging and cognition
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8036520/
https://www.ncbi.nlm.nih.gov/pubmed/33808221
http://dx.doi.org/10.3390/ijms22073574
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