The DOI matches its Crossref record; 96 of the 96 references it cites were found in a registry or an index.
Oxidative Stress in the Progression of Alzheimer Disease in the Frontal Cortex
Open accessAbstract
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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“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].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [31]
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“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]
Experimental — accuracy not yet measuredIn the citing paper
“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].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [31]
In the citing paper
“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].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [31]
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Current concepts in mild cognitive impairment
Petersen, R. C., Doody, R., Kurz, A., Mohs, R. C., Morris, J. C., Rabins, P. V., Ritchie, K., Rossor, M., Thal, L., & Winblad, B. (2001) · Archives of Neurology · doi:10.1001/archneur.58.12.1985 · Cited by 4,781
Reactive Oxygen Species and the Central Nervous System
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Oxidative Damage Is the Earliest Event in Alzheimer Disease
Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., et al. (2001) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/60.8.759 · Cited by 1,885
Mild Cognitive Impairment Represents Early-Stage Alzheimer Disease
Morris, J. C., Storandt, M., Miller, J. P., McKeel, D. W., Price, J. L., Rubin, E. H., & Berg, L. (2001) · Archives of Neurology · doi:10.1001/archneur.58.3.397 · Cited by 1,871
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Synaptic Activity Regulates Interstitial Fluid Amyloid-β Levels In Vivo
Cirrito, J. R., Yamada, K. A., Finn, M. B., Sloviter, R. S., Bales, K. R., May, P. C., Schoepp, D. D., Paul, S. M., Mennerick, S., & Holtzman, D. M. (2005) · Neuron · doi:10.1016/j.neuron.2005.10.028 · Cited by 1,265
Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease
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Soluble oligomers of the amyloid β-protein impair synaptic plasticity and behavior
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Cited by
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Targeting oxidative stress in disease: Promise and limitations of antioxidant therapy
Forman, H. J., & Zhang, H. (2021) · Nature Reviews Drug Discovery · doi:10.1038/s41573-021-00233-1 · Cited by 2,900
Integrated Systems Approach Identifies Genetic Nodes and Networks in Late-Onset Alzheimer’s Disease
Zhang, B., Gaiteri, C., Bodea, L.-G., Wang, Z., McElwee, J., Podtelezhnikov, A. A., Zhang, C., Xie, T., Tran, L., Dobrin, R., et al. (2013) · Cell · doi:10.1016/j.cell.2013.03.030 · Cited by 1,657
Oxidative Stress in Neurodegenerative Diseases
Simonian, N. A., & Coyle, J. T. (1996) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pa.36.040196.000503 · Cited by 1,377
Metals, oxidative stress and neurodegenerative disorders
Jomová, K., Vondráková, D., Lawson, M. K., & Valko, M. (2010) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-010-0563-x · Cited by 1,074
Oxidative Stress and the Pathogenesis of Alzheimer's Disease
Zhao, Y., & Zhao, B. (2013) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2013/316523 · Cited by 855
Metadata
- 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
- 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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