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Cited by 113Glutathione Transferases and PolymorphismsAntioxidant Activity and Oxidative StressRedox biology and oxidative stress

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Oxidative stress and genetic markers of suboptimal antioxidant defense in the aging brain: a theoretical review

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Salminen, Lauren E., Paul, Robert H.·2014·Reviews in the Neurosciences
DOI 10.1515/revneuro-2014-0046PMC PMC6378111
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Abstract

Normal aging involves a gradual breakdown of physiological processes that leads to a decline in cognitive functions and brain integrity, yet the onset and progression of decline are variable among older individuals. While many biological changes may contribute to this degree of variability, oxidative stress is a key mechanism of the aging process that can cause direct damage to cellular architecture within the brain. Oligodendrocytes are at a high risk for oxidative damage due to their role in myelin maintenance and production and limited repair mechanisms, suggesting that white matter may be particularly vulnerable to oxidative activity. Antioxidant defense enzymes within the brain, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST), are crucial for breaking down the harmful end products of oxidative phosphorylation. Previous studies have revealed that allele variations of polymorphisms that encode these antioxidants are associated with abnormalities in SOD, CAT, GPx, and GST activity in the central nervous system. This review will focus on the role of oxidative stress in the aging brain and the impact of decreased antioxidant defense on brain integrity and cognitive function. Directions for future research investigations of antioxidant defense genes will also be discussed.

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Authors
Salminen, L. E., & Paul, R. H.
Affiliations
University of Missouri–St. Louis (US)
Corresponding author
Salminen, Lauren E.
ORCID
Venue
Reviews in the Neurosciences
Publisher
Walter de Gruyter GmbH
Published
2014-01-01
Volume
25
Issue
6
Pages
805-19
ISSN
  • 0334-1763 (ISSN-L)
  • 2191-0200
DOI
10.1515/revneuro-2014-0046
PMC
PMC6378111
OpenAlex
W2094909334
Cited by
113
References
194
Citations by year
2026: 6 · 2025: 8 · 2024: 10 · 2023: 9 · 2022: 8 · 2021: 21 · 2020: 10 · 2019: 7 · 2018: 5 · 2017: 7 · 2016: 11 · 2015: 11
FWCI
0.91
Type
journal article
Language
en
Open access
Licence
cc-by
Locations
  • Reviews in the Neurosciences (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (F31AG050450)
  • National Institute of Mental Health (R21MH090494)
  • National Institute of Neurological Disorders and Stroke (R01NS039538, R01NS052470)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Glutathione Transferases and Polymorphisms
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
oxidative stress, brain aging, antioxidant defense, genetic polymorphism, superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, oligodendrocytes, white matter, cognitive decline, brain integrity, gene-environment interaction
MeSH terms
Aging, Animals, Antioxidants, Brain, Brain Diseases, Cognition Disorders, Genetic Markers, Humans, Oxidative Stress

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