Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer's disease
Open accessAbstract
Increasing evidence supports a role for oxidative DNA damage in aging and several neurodegenerative diseases including Alzheimer's disease (AD). Attack of DNA by reactive oxygen species (ROS), particularly hydroxyl radicals, can lead to strand breaks, DNA-DNA and DNA-protein cross-linking, and formation of at least 20 modified bases adducts. In addition, alpha,beta-unsaturated aldehydic by-products of lipid peroxidation including 4-hydroxynonenal and acrolein can interact with DNA bases leading to the formation of bulky exocyclic adducts. Modification of DNA bases by direct interaction with ROS or aldehydes can lead to mutations and altered protein synthesis. Several studies of DNA base adducts in late-stage AD (LAD) brain show elevations of 8-hydroxyguanine (8-OHG), 8-hydroxyadenine (8-OHA), 5-hydroxycytosine (5-OHC), and 5-hydroxyuracil, a chemical degradation product of cytosine, in both nuclear and mitochondrial DNA (mtDNA) isolated from vulnerable regions of LAD brain compared to age-matched normal control subjects. Previous studies also show elevations of acrolein/guanine adducts in the hippocampus of LAD subjects compared to age-matched controls. In addition, studies of base excision repair show a decline in repair of 8-OHG in vulnerable regions of LAD brain. Our recent studies show elevated 8-OHG, 8-OHA, and 5,6-diamino-5-formamidopyrimidine in both nuclear and mtDNA isolated from vulnerable brain regions in amnestic mild cognitive impairment, the earliest clinical manifestation of AD, suggesting that oxidative DNA damage is an early event in AD and is not merely a secondary phenomenon.
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Increased DNA oxidation is observed in post mortem AD brain, MCI, and preclinical AD, and may exacerbate AD progression.
“Increased DNA oxidation was observed in post mortem AD brain [496], MCI [497], and preclinical AD [498], and may exacerbate AD progression [499, 500].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [497]
Accumulation of DNA damage has been shown to predict progression from mild cognitive impairment to AD prior to the emergence of any neuropathology.
“accumulation of DNA damage has been shown to predict progression from mild cognitive impairment (MCI) to AD prior to the emergence of any neuropathology [91].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [91]
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Nuclear and mitochondrial DNA oxidation in Alzheimer's disease
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DNA Damage-Induced Neurodegeneration in Accelerated Ageing and Alzheimer’s Disease
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Mitochondrial Function and Neurodegenerative Diseases
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- Authors
- Lovell, M. A., & Markesbery, W. R.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Lovell, M. A.
- ORCID
- Lovell, M. A.
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-11-26
- Volume
- 35
- Issue
- 22
- Pages
- 7497-7504
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC2190704
- OpenAlex
- W1967899016
- Cited by
- 515
- References
- 78
- Citations by year
- 2026: 18 · 2025: 23 · 2024: 25 · 2023: 31 · 2022: 39 · 2021: 35 · 2020: 32 · 2019: 25 · 2018: 20 · 2017: 27 · 2016: 21 · 2015: 26 · 2014: 19 · 2013: 25 · 2012: 29
- FWCI
- 2.95
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nucleic Acids Research (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by-nc)
- Funders
- National Institute on Aging (P30AG028383, P01AG005119)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- oxidative DNA damage, Alzheimer's disease, mild cognitive impairment, reactive oxygen species, hydroxyl radicals, DNA base adducts, 8-oxoguanine, 5-hydroxycytosine, 4-hydroxynonenal, acrolein, lipid peroxidation, mitochondrial DNA, base excision repair, hippocampus, aging
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cognition Disorders, DNA, DNA Damage, DNA Repair, Humans, Oxidation-Reduction, Oxidative Stress
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