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Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair
Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed in all tissues, the brain being the most important one due to its main role in the homeostasis of the orga...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743731/ https://www.ncbi.nlm.nih.gov/pubmed/29311911 http://dx.doi.org/10.3389/fnagi.2017.00430 |
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author | Zárate, Sandra Stevnsner, Tinna Gredilla, Ricardo |
author_facet | Zárate, Sandra Stevnsner, Tinna Gredilla, Ricardo |
author_sort | Zárate, Sandra |
collection | PubMed |
description | Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed in all tissues, the brain being the most important one due to its main role in the homeostasis of the organism. As our knowledge about the underlying mechanisms of brain aging increases, potential approaches to preserve brain function rise significantly. Accumulating evidence suggests that loss of genomic maintenance may contribute to aging, especially in the central nervous system (CNS) owing to its low DNA repair capacity. Sex hormones, particularly estrogens, possess potent antioxidant properties and play important roles in maintaining normal reproductive and non-reproductive functions. They exert neuroprotective actions and their loss during aging and natural or surgical menopause is associated with mitochondrial dysfunction, neuroinflammation, synaptic decline, cognitive impairment and increased risk of age-related disorders. Moreover, loss of sex hormones has been suggested to promote an accelerated aging phenotype eventually leading to the development of brain hypometabolism, a feature often observed in menopausal women and prodromal Alzheimer’s disease (AD). Although data on the relation between sex hormones and DNA repair mechanisms in the brain is still limited, various investigations have linked sex hormone levels with different DNA repair enzymes. Here, we review estrogen anti-aging and neuroprotective mechanisms, which are currently an area of intense study, together with the effect they may have on the DNA repair capacity in the brain. |
format | Online Article Text |
id | pubmed-5743731 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-57437312018-01-08 Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair Zárate, Sandra Stevnsner, Tinna Gredilla, Ricardo Front Aging Neurosci Neuroscience Aging is an inevitable biological process characterized by a progressive decline in physiological function and increased susceptibility to disease. The detrimental effects of aging are observed in all tissues, the brain being the most important one due to its main role in the homeostasis of the organism. As our knowledge about the underlying mechanisms of brain aging increases, potential approaches to preserve brain function rise significantly. Accumulating evidence suggests that loss of genomic maintenance may contribute to aging, especially in the central nervous system (CNS) owing to its low DNA repair capacity. Sex hormones, particularly estrogens, possess potent antioxidant properties and play important roles in maintaining normal reproductive and non-reproductive functions. They exert neuroprotective actions and their loss during aging and natural or surgical menopause is associated with mitochondrial dysfunction, neuroinflammation, synaptic decline, cognitive impairment and increased risk of age-related disorders. Moreover, loss of sex hormones has been suggested to promote an accelerated aging phenotype eventually leading to the development of brain hypometabolism, a feature often observed in menopausal women and prodromal Alzheimer’s disease (AD). Although data on the relation between sex hormones and DNA repair mechanisms in the brain is still limited, various investigations have linked sex hormone levels with different DNA repair enzymes. Here, we review estrogen anti-aging and neuroprotective mechanisms, which are currently an area of intense study, together with the effect they may have on the DNA repair capacity in the brain. Frontiers Media S.A. 2017-12-22 /pmc/articles/PMC5743731/ /pubmed/29311911 http://dx.doi.org/10.3389/fnagi.2017.00430 Text en Copyright © 2017 Zárate, Stevnsner and Gredilla. http://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) or licensor 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 Zárate, Sandra Stevnsner, Tinna Gredilla, Ricardo Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title | Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title_full | Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title_fullStr | Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title_full_unstemmed | Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title_short | Role of Estrogen and Other Sex Hormones in Brain Aging. Neuroprotection and DNA Repair |
title_sort | role of estrogen and other sex hormones in brain aging. neuroprotection and dna repair |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5743731/ https://www.ncbi.nlm.nih.gov/pubmed/29311911 http://dx.doi.org/10.3389/fnagi.2017.00430 |
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