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Int. J. Mol. Sci. 2012, 13(12), 16172-16222; doi:10.3390/ijms131216172
Review

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

,
 and *
Institute for Veterinary Biochemistry and Molecular Biology, University of Zürich-Irchel, Winterthurerstrasse 190, 8057 Zürich, Switzerland These authors contributed equally to this work.
* Author to whom correspondence should be addressed.
Received: 21 September 2012 / Revised: 6 November 2012 / Accepted: 12 November 2012 / Published: 30 November 2012
(This article belongs to the Special Issue DNA Damage and Repair in Degenerative Diseases)
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Abstract

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.
Keywords: brain; neurodegeneration; reactive oxygen species; DNA damage; base excision repair brain; neurodegeneration; reactive oxygen species; DNA damage; base excision repair
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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MDPI and ACS Style

Bosshard, M.; Markkanen, E.; van Loon, B. Base Excision Repair in Physiology and Pathology of the Central Nervous System. Int. J. Mol. Sci. 2012, 13, 16172-16222.

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