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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“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]
In the citing paper
“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]
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Cites
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Items 101–132 of 132
Ansari, M. A., Rao, M. S. R., Al‐Jarallah, A., & Babiker, F. A. (2022) · Brain Research · doi:10.1016/j.brainres.2022.148134 · Cited by 15
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Thioxanthenes, chlorprothixene and flupentixol inhibit proton currents in BV2 microglial cells
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Ravelli, K. G., Rosário, B. D. A., Vasconcelos, A. R., Scavone, C., Camarini, R., Hernandes, M. S., & Britto, L. R. (2017) · Neuroscience · doi:10.1016/j.neuroscience.2017.06.050 · Cited by 11
“Mild cognitive impairment and early AD are characterized by loss of synapses and connectivity, which occurs in parallel with NADPH-oxidase upregulation (mainly Nox2) in frontal and temporal cortex (Ansari and Scheff, 2011).”
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BackgroundBen‐Azu, B., Oghorodi, A. M., Oritsemuelebi, B., & Chidebe, E. O. (2024) · IntechOpen eBooks · doi:10.5772/intechopen.112517 · Cited by 9
The Alzheimer’s Disease Brain, Its Microvasculature, and NADPH Oxidase
Mamelak, M. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230415 · Cited by 10
“Most important, an inverse correlation was observed between NOX activity and cognitive ability [34].”
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Targeting NOX2: An In-Silico approach with Phytoconstituents to Alleviate Oxidative Stress
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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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