Cited by 112Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchMitochondrial Function and Pathology

Nucleic acid oxidation: an early feature of Alzheimer's disease

Open access
Bradley‐Whitman, Melissa A., Timmons, Michael D., Beckett, Tina L., Murphy, Michael P., Lynn, Bert C., Lovell, Mark A.·2014·Journal of Neurochemistry

Abstract

Studies of oxidative damage during the progression of Alzheimer's disease (AD) suggest its central role in disease pathogenesis. To investigate levels of nucleic acid oxidation in both early and late stages of AD, levels of multiple base adducts were quantified in nuclear and mitochondrial DNA from the superior and middle temporal gyri (SMTG), inferior parietal lobule (IPL), and cerebellum (CER) of age‐matched normal control subjects, subjects with mild cognitive impairment, preclinical AD, late‐stage AD, and non‐AD neurological disorders (diseased control; DC) using gas chromatography/mass spectrometry. Median levels of multiple DNA adducts in nuclear and mitochondrial DNA were significantly (p ≤ 0.05) elevated in the SMTG, IPL, and CER in multiple stages of AD and in DC subjects. Elevated levels of fapyguanine and fapyadenine in mitochondrial DNA suggest a hypoxic environment early in the progression of AD and in DC subjects. Overall, these data suggest that oxidative damage is an early event not only in the pathogenesis of AD but is also present in neurodegenerative diseases in general. image Levels of oxidized nucleic acids in nDNA and mtDNA were found to be significantly elevated in mild cognitive impairment (MCI), preclinical Alzheimer's disease (PCAD), late‐stage AD (LAD), and a pooled diseased control group (DC) of frontotemporal dementia (FTD) and dementia with Lewy bodies (DLB) subjects compared to normal control (NC) subjects. Nucleic acid oxidation peaked early in disease progression and remained elevated. The study suggests nucleic acid oxidation is a general event in neurodegeneration.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1111/jnc.12444

Cites

87 of 87 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

Authors
Bradley‐Whitman, M. A., Timmons, M. D., Beckett, T. L., Murphy, M. P., Lynn, B. C., & Lovell, M. A.
Affiliations
University of Kentucky (US)
Corresponding author
Lovell, Mark A.
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2013-10-21
Volume
128
Issue
2
Pages
294-304
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2155515447
Cited by
112
References
87
Citations by year
2026: 5 · 2025: 11 · 2024: 7 · 2023: 8 · 2022: 10 · 2021: 14 · 2020: 13 · 2019: 8 · 2018: 7 · 2017: 5 · 2016: 11 · 2015: 5 · 2014: 8
FWCI
5.51
Type
journal article
Language
en
Open access
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
NIH (5P01-AG05119, P30-AG028383)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
Alzheimer's disease, nucleic acid oxidation, oxidative DNA damage, DNA adducts, mitochondrial DNA, nuclear DNA, hypoxia, mild cognitive impairment, preclinical Alzheimer's disease, frontotemporal dementia, dementia with Lewy bodies, neurodegeneration, temporal lobe, cerebellum
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Brain, Cell Nucleus, DNA, DNA Damage, DNA, Mitochondrial, Female, Humans, Male, Oxidation-Reduction, Case-Control Studies, DNA Adducts, Lewy Body Disease, Frontotemporal Dementia

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review