Base Excision Repair in Physiology and Pathology of the Central Nervous System

Relatively low levels of antioxidant enzymes and high oxygen metabolism result in formation of numerous oxidized DNA lesions in the tissues of the central nervous system. Accumulation of damage in the DNA, due to continuous genotoxic stress, has been linked to both aging and the development of vario...

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Autores principales: Bosshard, Matthias, Markkanen, Enni, van Loon, Barbara
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Molecular Diversity Preservation International (MDPI) 2012
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546685/
https://www.ncbi.nlm.nih.gov/pubmed/23203191
http://dx.doi.org/10.3390/ijms131216172
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author Bosshard, Matthias
Markkanen, Enni
van Loon, Barbara
author_facet Bosshard, Matthias
Markkanen, Enni
van Loon, Barbara
author_sort Bosshard, Matthias
collection PubMed
description Relatively low levels of antioxidant enzymes and high oxygen metabolism result in formation of numerous oxidized DNA lesions in the tissues of the central nervous system. Accumulation of damage in the DNA, due to continuous genotoxic stress, has been linked to both aging and the development of various neurodegenerative disorders. Different DNA repair pathways have evolved to successfully act on damaged DNA and prevent genomic instability. The predominant and essential DNA repair pathway for the removal of small DNA base lesions is base excision repair (BER). In this review we will discuss the current knowledge on the involvement of BER proteins in the maintenance of genetic stability in different brain regions and how changes in the levels of these proteins contribute to aging and the onset of neurodegenerative disorders.
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spelling pubmed-35466852013-01-23 Base Excision Repair in Physiology and Pathology of the Central Nervous System Bosshard, Matthias Markkanen, Enni van Loon, Barbara Int J Mol Sci Review Relatively low levels of antioxidant enzymes and high oxygen metabolism result in formation of numerous oxidized DNA lesions in the tissues of the central nervous system. Accumulation of damage in the DNA, due to continuous genotoxic stress, has been linked to both aging and the development of various neurodegenerative disorders. Different DNA repair pathways have evolved to successfully act on damaged DNA and prevent genomic instability. The predominant and essential DNA repair pathway for the removal of small DNA base lesions is base excision repair (BER). In this review we will discuss the current knowledge on the involvement of BER proteins in the maintenance of genetic stability in different brain regions and how changes in the levels of these proteins contribute to aging and the onset of neurodegenerative disorders. Molecular Diversity Preservation International (MDPI) 2012-11-30 /pmc/articles/PMC3546685/ /pubmed/23203191 http://dx.doi.org/10.3390/ijms131216172 Text en © 2012 by the authors; licensee Molecular Diversity Preservation International, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Bosshard, Matthias
Markkanen, Enni
van Loon, Barbara
Base Excision Repair in Physiology and Pathology of the Central Nervous System
title Base Excision Repair in Physiology and Pathology of the Central Nervous System
title_full Base Excision Repair in Physiology and Pathology of the Central Nervous System
title_fullStr Base Excision Repair in Physiology and Pathology of the Central Nervous System
title_full_unstemmed Base Excision Repair in Physiology and Pathology of the Central Nervous System
title_short Base Excision Repair in Physiology and Pathology of the Central Nervous System
title_sort base excision repair in physiology and pathology of the central nervous system
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546685/
https://www.ncbi.nlm.nih.gov/pubmed/23203191
http://dx.doi.org/10.3390/ijms131216172
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