The DOI matches its Crossref record; 43 of the 43 references it cites were found in a registry or an index.
NADPH-oxidase activation and cognition in Alzheimer disease progression
Open accessAbstract
Superoxide production via NADPH-oxidase (NOX) has been shown to play a role in a variety of neurological disorders, including Alzheimer disease (AD). To improve our understanding of the NOX system and cognitive impairment, we studied the various protein components of the phagocytic isoform (gp91(phox), or NOX2) in the frontal and temporal cortex of age- and postmortem-matched samples. Individuals underwent antemortem cognitive testing and postmortem histopathologic assessment to determine disease progression and assignment to one of the following groups: no cognitive impairment (NCI), preclinical AD, mild cognitive impairment (MCI), early AD, and mild-to-moderate AD. Biochemical methods were used to determine overall NOX activity as well as levels of the various subunits (gp91(phox), p67(phox), p47(phox), p40(phox), and p22(phox)). Overall enzyme activity was significantly elevated in the MCI cohort in both cortical regions compared to the NCI cohort. This activity level remained elevated in the AD groups. Only the NOX cytosolic subunit proteins (p67(phox), p47(phox), and p40(phox) ) were significantly elevated with disease progression; the membrane-bound subunits (gp91(phox) and p22(phox)) remained stable. In addition, there was a robust correlation between NOX activity and the individual's cognitive status such that as the enzyme activity increased, cognitive performance decreased. Collectively, these data show that upregulated NADPH-oxidase in frontal and temporal cortex suggests that increases in NOX-associated redox pathways might participate in early pathogenesis and contribute to AD progression.
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“Past and recent studies have demonstrated that oxidative damage is not only an early event in the pathogenesis of AD, occurring before the onset of clinical symptoms but also a factor contributing to the disease progression [17,18,19,20,21].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [21]
Experimental — accuracy not yet measuredIn the citing paper
“Furthermore, ante-mortem cognitive impairment is correlated with post-mortem determination of NOX activity in the frontal and temporal cortices [68].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [68]
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Cites
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“One of the presumed early transition stages is the clinical diagnosis of mild cognitive impairment (MCI), defined as an individual expressing consistent, measurable memory impairment without dementia or significant disability related to activities of daily living [3, 4].”
BackgroundNOX enzymes and the biology of reactive oxygen
Lambeth, J. D. (2004) · Nature Reviews Immunology · doi:10.1038/nri1312 · Cited by 3,125
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Self-citationOxidative Damage Is the Earliest Event in Alzheimer Disease
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“Excessive amounts of ROS can be extremely detrimental resulting in elevated levels of oxidative stress that appear to play an important role in numerous degenerative diseases including AD [8, 26, 27].”
BackgroundMild Cognitive Impairment as a Clinical Entity and Treatment Target
Petersen, R. C., & Morris, J. C. (2005) · Archives of Neurology · doi:10.1001/archneur.62.7.1160 · Cited by 935 · cited 2×
“One of the presumed early transition stages is the clinical diagnosis of mild cognitive impairment (MCI), defined as an individual expressing consistent, measurable memory impairment without dementia or significant disability related to activities of daily living [3, 4].”
BackgroundMethodBABIOR, B. M., Lambeth, J. D., & Nauseef, W. M. (2002) · Archives of Biochemistry and Biophysics · doi:10.1006/abbi.2001.2642 · Cited by 911 · cited 1×
“Brain phagocytes have a NOX complex that is composed of primarily five different subunits [14].”
BackgroundSome morphometric aspects of the brain in senile dementia of the alzheimer type
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“Based on these observations, the term “antagonistic pleiotropy” has been coined to explain a potential role of NOX in the brain [24].”
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Cited by
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Simpson, D. S. A., & Oliver, P. L. (2020) · Antioxidants · doi:10.3390/antiox9080743 · Cited by 1,044
NADPH oxidase in brain injury and neurodegenerative disorders
Ma, M. W., Wang, J., Zhang, Q., Wang, R., Dhandapani, K. M., Vadlamudi, R. K., & Brann, D. W. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0150-7 · Cited by 432
The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders
Tarafdar, A., & Pula, G. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19123824 · Cited by 373
“Additionally, not only were NOX cytosolic subunits significantly elevated compared to the membrane bound subunits but with increased NOX activity cognitive performance of the individual also decreased [16].”
BackgroundNew Insights on NOX Enzymes in the Central Nervous System
Nayernia, Z., Jaquet, V., & Krause, K.-H. (2014) · Antioxidants & Redox Signaling · doi:10.1089/ars.2013.5703 · Cited by 279
“Inter-estingly, cytosolic subunits (p67 phox , p47 phox , and p40 phox ) were increased, but not NOX2 (6).”
Manganese Superoxide Dismutase and Oxidative Stress Modulation
Bresciani, G., da Cruz, I. B. M., & González‐Gallego, J. (2015) · Advances in clinical chemistry · doi:10.1016/bs.acc.2014.11.001 · Cited by 284
“The O2 • anion production via NADPH-oxidase (NOX) plays a role in a variety of neurological diseases, including AD [121].”
Background
Metadata
- Authors
- Ansari, M. A., & Scheff, S. W.
- Affiliations
- University of Kentucky (US)
- Corresponding author
- Scheff, Stephen W.
- ORCID
- Ansari, Mubeen A.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 51
- Issue
- 1
- Pages
- 171-178
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3109185
- OpenAlex
- W2068872788
- Cited by
- 131
- References
- 43
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 9 · 2023: 9 · 2022: 7 · 2021: 15 · 2020: 13 · 2019: 7 · 2018: 7 · 2017: 8 · 2016: 9 · 2015: 6 · 2014: 12 · 2013: 9 · 2012: 10
- FWCI
- 7.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG27219, PO1 AG14449, AG028383)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- NADPH oxidase, Alzheimer's disease, cognitive impairment, mild cognitive impairment, superoxide production, gp91phox, p67phox, p47phox, p40phox, p22phox, frontal cortex, temporal cortex, redox pathways, disease progression, postmortem brain
- MeSH terms
- NADPH Oxidase 2, Aged, Aged, 80 and over, Alzheimer Disease, Cognition, Enzyme Activation, Female, Humans, Male, Membrane Glycoproteins, Superoxides, Blotting, Western, Oxidative Stress, Disease Progression, NADPH Oxidases
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