Cited by 623Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchAntioxidant Activity and Oxidative Stress

Oxidative stress in the progression of Alzheimer disease in the frontal cortex

Open access
Ansari, Mubeen A., Scheff, Stephen W.·2010·Journal of Neuropathology & Experimental Neurology

Abstract

We investigated oxidative stress in human postmortem frontal cortexfrom individuals characterized as mild cognitive impairment (n= 8), mild/moderate Alzheimer disease (n = 4), and late-stage Alzheimer disease (n = 9). Samples from subjects with no cognitive impairment (n = 10) that were age- and postmortem interval-matched with these cases were used as controls. The short postmortem intervalbrain samples were processed for postmitochondrial supernatant, nonsynaptic mitochondria, and synaptosome fractions. Samples were analyzed for several antioxidants (glutathione, glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, superoxide dismutase, catalase) and the oxidative marker, thiobarbituric acid reactive substances. The tissue was also analyzed for possible changes in protein damage using neurochemical markers for protein carbonyls, 3-nitrotyrosine, 4-hydroxynonenal, andacrolein. All 3 neuropil fractions (postmitochondrial supernatant, mitochondrial, and synaptosomal) demonstrated significant disease-dependent increases in oxidative markers. The highest changes were observed in the synaptosomal fraction. Both mitochondrial and synaptosomal fractions had significant declines in antioxidants (glutathione, glutathione peroxidase, glutathione-S-transferase, and superoxide dismutase). Levels of oxidative markers significantly correlated with Mini-Mental Status Examination scores. Oxidative stress was more localized to the synapses, with levels increasing in a disease-dependent fashion. These correlations implicate an involvement of oxidative stress in Alzheimer disease-related synaptic loss.

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 · 10.1097/nen.0b013e3181cb5af4

Cites

96 of 96 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?

  • Tunneling nanotube formation is often associated with oxidative stress, another key feature of Alzheimer's disease.

    “Moreover, TNT formation is often associated with oxidative stress, another key feature of AD [120,121,122].”

    From The Impact of Neurotoxin Proteins Trafficked by Primary Cilia and Extracellular Vesicles in Neurodegenerative Diseases (2025) · cites this paper as [121]

    The Discussion reports that oxidative stress increases with Alzheimer disease progression, supporting its description as a feature of AD. The paper does not address tunneling nanotubes or an association between their formation and oxidative stress. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • 3-Nitrotyrosine and protein carbonyls are used as biomarkers of oxidative damage in the brain of Alzheimer's disease and mild cognitive impairment.

    “3-nitrotyrosine and protein carbonyls, these last produced mainly by the action of free radicals on the peptide chain or by oxidation of amino acids, are used as biomarkers of oxidative damage in the brain of AD and MCI [18,24,31,32,33].”
  • In response to OS in the brain, compensatory induction of antioxidant enzymes such as superoxide dismutase, glutathione reductase, catalase has been found in vulnerable neurons in AD.

    “In response to OS in the brain, a number of protective mechanisms are up regulated to maintain the oxidative balance, in particular compensatory induction of antioxidant enzymes such as superoxide dismutase, glutathione reductase, catalase have been found in vulnerable neurons in AD [31].”
  • Reduction of antioxidants such as glutathione, glutathione peroxidase, glutathione-S-transferase, and superoxide dismutase is demonstrated post-mortem in mitochondrial and synaptosomal fractions in the frontal cortex of MCI and AD patients.

    “Reduction of antioxidants such as glutathione, glutathione peroxidase, glutathione-S-transferase, and superoxide dismutase are demonstrated post-mortem in the mitochondrial and synaptosomal fractions in the frontal cortex of MCI and AD patients [31].”

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
Ansari, M. A., & Scheff, S. W.
Affiliations
University of Kentucky (US)
Corresponding author
Scheff, Stephen W.
Venue
Journal of Neuropathology & Experimental Neurology
Published
2010-02
Volume
69
Issue
2
Pages
155-167
ISSN
  • 0022-3069 (ISSN-L)
  • 1554-6578
OpenAlex
W2031762170
Cited by
605
References
96
Citations by year
2026: 29 · 2025: 38 · 2024: 44 · 2023: 40 · 2022: 51 · 2021: 56 · 2020: 44 · 2019: 38 · 2018: 30 · 2017: 31 · 2016: 41 · 2015: 29 · 2014: 31 · 2013: 24 · 2012: 31
FWCI
21.61
Type
journal article
Language
en
Open access
Locations
  • Journal of Neuropathology & Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute on Aging (AG-028383, AG27219, P30AG028383, P01AG014449, R01AG043375, R01AG027219)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
Keywords
oxidative stress, Alzheimer's disease, frontal cortex, synaptosomes, mitochondria, antioxidants, glutathione, superoxide dismutase, lipid peroxidation, protein carbonyls, nitrotyrosine, 4-hydroxynonenal, acrolein, synaptic loss, disease progression, mild cognitive impairment, postmortem brain
MeSH terms
Aged, Aged, 80 and over, Aldehydes, Alzheimer Disease, Antioxidants, Female, Frontal Lobe, Humans, Male, Mental Status Schedule, Synapses, Tissue Distribution, Tyrosine, Biomarkers, Thiobarbituric Acid Reactive Substances, Oxidative Stress, Disease Progression, Protein Carbonylation

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