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

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Oxidative Stress in the Progression of Alzheimer Disease in the Frontal Cortex

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

DOI 10.1097/nen.0b013e3181cb5af4PMC PMC2826839

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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.

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Authors: Ansari, M. A., & Scheff, S. W.
Affiliations: University of Kentucky (US)
Corresponding author: Scheff, Stephen W.
ORCID: Ansari, Mubeen A.
Venue: Journal of Neuropathology & Experimental Neurology
Publisher: Oxford University Press (OUP)
Published: 2010-02
Volume: 69
Issue: 2
Pages: 155-167
ISSN: 0022-3069 (ISSN-L)
1554-6578
DOI: 10.1097/nen.0b013e3181cb5af4
PMC: PMC2826839
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: green
www.ncbi.nlm.nih.gov
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: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Health Sciences › Medicine › Biochemistry (medical) › 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

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Oxidative Stress in the Progression of Alzheimer Disease in the Frontal Cortex

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