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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]
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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]
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Background
Cited by
Sorted by citations
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Manganese Superoxide Dismutase and Oxidative Stress Modulation
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Old Maids: Aging and Its Impact on Microglia Function
Koellhoffer, E. C., McCullough, L. D., & Ritzel, R. M. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18040769 · Cited by 213
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“However, male’s cardiac mitochondria exhibited fragmented, circular, and smaller mitochondria relative to female’s mitochondria, while no morphologic sex-dependent differences were observed in cortical mitochondria.”
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“In AD patients, during the initial stages of the disease, the expression of all 3 isoforms of NOX was shown to be significantly increased [226], activating NOX-associated pathways and contributing to AD progression [45].”
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“Furthermore, NOX has been identified as the key source of O2 ̅ that contributes to cardiovascular aging [11] and other age-associated conditions such as diabetes [22], arthritis [23], cataracts [24], Alzheimer’s disease [25] and motorneuron dysfunction [10].”
BackgroundTargeting microglia-mediated neurotoxicity: the potential of NOX2 inhibitors
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BackgroundWhich NADPH Oxidase Isoform Is Relevant for Ischemic Stroke? The Case for Nox 2
Kahles, T., & Brandes, R. P. (2013) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.4721 · Cited by 125
“Conversely, some of the oxidized proteins themselves activate and induce Nox proteins as observed in the brains of AD patients (8, 26) or in response to the amyloid b (Ab) and amyloid precursor protein (APP).”
BackgroundBamburg, J. R., Minamide, L. S., Wiggan, O., Tahtamouni, L. H., & Kuhn, T. B. (2021) · Cells · doi:10.3390/cells10102726 · Cited by 124
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“NADPH oxidase (NOX) and mitochondria-derived ROS are known to augment pro-inflammatory events in activated microglia, particularly in neurodegenerative disorders, such as PD, AD, ALS and multiple sclerosis (Ansari and Scheff 2011; Cristovao et al. 2012; Zhang et al. 2014).”
Hajipour, S., Sarkaki, A., Farbood, Y., Eidi, A., Mortazavi, P., & Valizadeh, Z. (2016) · Basic and Clinical Neuroscience Journal · doi:10.15412/j.bcn.03070203 · Cited by 109
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“NADPH oxidase, a superoxide-producing enzyme, is composed of membrane (gp91 phox, p22 phox) and cytosolic (p47 phox, p67 phox, p40 phox and Rac1/2) subunits (Ansari and Scheff, 2011; Guemez-Gamboa et al., 2011; Khalyfa et al., 2014).”
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NADPH oxidases: redox regulation of cell homeostasis and disease
Kračun, D., Lopes, L. R., Cifuentes-Pagano, E., & Pagano, P. J. (2025) · Physiological Reviews · doi:10.1152/physrev.00034.2023 · Cited by 114
Oxidative Stress and Gut-Derived Lipopolysaccharides in Neurodegenerative Disease: Role of NOX2
Loffredo, L., Ettorre, E., Zicari, A. M., Inghilleri, M., Nocella, C., Perri, L., Spalice, A., Fossati, C., De Lucia, M. C., Pigozzi, F., et al. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/8630275 · Cited by 100
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“…2001) and multiple studies have reported oxidative stress is significantly elevated in several brain regions of aMCI individuals (Ansari and Scheff, 2010,Ansari and Scheff, 2011,Butterfield, et al., 2006,Keller, et al., 2005,Markesbery, et al., 2005,Pratico and Sung, 2004,Williams, et al., 2006).”
InfluentialSelf-citationCognitive impairment in humanized APP×PS1 mice is linked to Aβ1–42 and NOX activation
Bruce-Keller, A. J., Gupta, S., Knight, A. G., Beckett, T. L., McMullen, J. M., Davis, P. R., Murphy, M. P., Van Eldik, L. J., St Clair, D., & Keller, J. N. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.07.012 · Cited by 96
“Overall, these data are in general agreement with published studies suggesting a role for NOX in the pathogenesis of AD (Ansari and Scheff, 2011), (Park et al., 2008), (Bruce-Keller et al., 2010), but extend these Neurobiol Dis.”
InfluentialNOX2 As a Target for Drug Development: Indications, Possible Complications, and Progress
Diebold, B. A., Smith, S. M., Yang, L., & Lambeth, J. D. (2014) · Antioxidants and Redox Signaling · doi:10.1089/ars.2014.5862 · Cited by 99
“Biochemical studies showed increased p47phox and p67phox in membrane fractions from human AD postmortem cortices as well as increased NOX2 activity in brain cortex homogenates compared with age-matched non-diseased brains (10, 270).”
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“Moreover, the neurodegenerative Huntington’s (164), Alzheimer’s (9), and Parkinson’s diseases have augmented ROS implicated in their etiology (27, 154).”
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Amyloid β‐induced astrogliosis is mediated by β1‐integrin via NADPH oxidase 2 in Alzheimer's disease
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“Unlike our results, the NOX activation in AD brains was exclusively attributed to microglial cells (Ansari and Scheff, 2011) and not to astrocytes or neurons.”
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“Significantly, the authors found an inverse correlation between Frontiers in Neuroscience | www.frontiersin.org 4 February 2019 | Volume 13 | Article 48 postmortem NOX activity and ante-mortem cognitive status (Ansari and Scheff, 2011).”
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Sorce, S., Krause, K., & Jaquet, V. (2012) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-012-1014-5 · Cited by 79
“p h o sp h o ry la ti o n ) [3 4 ]”
BackgroundInfluentialGinsenoside Rg1 alleviates Aβ deposition by inhibiting NADPH oxidase 2 activation in APP/PS1 mice
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“In the brain, NOX2 is mainly expressed in neurons and is closely involved in the progression of AD [44].”
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Uddin, M. S., Kabir, M. T., Jalouli, M., Rahman, M. A., Jeandet, P., Behl, T., Alexiou, A. T., Albadrani, G. M., Abdel‐Daim, M. M., Perveen, A., et al. (2021) · Current Neuropharmacology · doi:10.2174/1570159x19666210826130210 · Cited by 76
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“Importantly, it has also been reported that in the frontal and temporal cortical regions of individuals with mild cognitive impairment, as well as in AD patients, NOX2 oxidase activity and cytosolic subunit expression are elevated in these regions when studied post-mortem (Ansari and Scheff 2011).”
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“NOX‑2 and NOX‑4, as the major NADPH oxidase isoform expressed in the tissue samples, are principal sources of oxidative stress (41,42).”
The neuroprotective effects of apocynin
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“Interestingly, NADPH-oxidase has been found to be upregulated in the frontal and temporal cortex, which suggests that elevated NOX-associated redox pathways may play an integral part in the progression of dementia [50].”
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Santos, R. X., Correia, S. C., Zhu, X., Lee, H.-G., Petersen, R. B., Nunomura, A., Smith, M. A., Perry, G., & Moreira, P. I. (2012) · Free Radical Research · doi:10.3109/10715762.2011.648188 · Cited by 57
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Inflamma-MicroRNAs in Alzheimer’s Disease: From Disease Pathogenesis to Therapeutic Potentials
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“MicroRNAs (miRNAs) are a class of endogenous short sequence non-coding RNAs that indirectly inhibit translation or directly degrade messenger RNA (mRNA) by specifically binding to its 3′ untranslated region (UTR).”
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“The expression of NOX2 subunits p47phox and p67phox are also increased in the cortex of patients with mild cognitive disorders (5).”
BackgroundOxidative Stress: Pathological Driver in Chronic Neurodegenerative Diseases
Chong, Z. Z., & Souayah, N. (2025) · Antioxidants · doi:10.3390/antiox14060696 · Cited by 50
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“Oxidative stress has been closely correlated with global cognitive status and impli‐ cated in the neuronal death in AD (Ansari & Scheff, 2011; Ferreiro et al., 2012).”
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Implication of type 4 NADPH oxidase (NOX4) in tauopathy
Luengo, E., Trigo-Alonso, P., Fernández‐Mendívil, C., Núñez, Á., del Campo, M., Porrero, C., García‐Magro, N., Negredo, P., Senar, S., Sánchez‐Ramos, C., et al. (2021) · Free Radical Biology and Medicine · doi:10.1016/j.redox.2021.102210 · Cited by 44
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“NOX is up-regulated with the translocation/interaction of its cytosolic proteins to the membrane subunit [29,31,50,54] and subsequently participates in various pathophysiological mechanisms [48,50,54-58].”
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“AD postmortem brains p67phox, p47phox, and p40phox Increasing of redox pathways [126]”
BackgroundInfluentialChronic hypoxia of endothelial cells boosts HIF-1α-NLRP1 circuit in Alzheimer’s disease
Jung, E., Kim, Y. E., Jeon, H. S., Yoo, M., Kim, M., Kim, Y., Koh, S., & Choi, Y. K. (2023) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2023.05.011 · Cited by 40
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“In rat and mouse models without or with some treatment in which the activity of NADPH oxidase is shown, the expression and activity of NOX2 and NOX4 have been reported in the hippocampus and cortex, important areas of the brain related to memory and learning [85].”
BackgroundBridged tetrahydroisoquinolines as selective NADPH oxidase 2 (Nox2) inhibitors
Cifuentes-Pagano, E., Saha, J., Csányi, G., Ghouleh, I. A., Sahoo, S., Rodriguez, A. I., Wipf, P., Pagano, P. J., & Skoda, E. M. (2013) · MedChemComm · doi:10.1039/c3md00061c · Cited by 39
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Xu, T., Sun, L., Shen, X., Chen, Y., Yin, Y., Zhang, J., Huang, D., Li, W., & Li, W. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.01.025 · Cited by 38
The Role of Vitamin D in Alzheimer’s Disease
Lương, K. V. Q., & Nguyễn, L. (2013) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317512473196 · Cited by 37
“The NOX is also upregulated in the frontal and temporal cortex and contributes to AD progression.(169) The inhibition of NOX or the gene deletion of its functional p47 subunit promotes alternative and anti-inflammatory microglial activation during neuroinflammation.”
BackgroundSun, L., Chen, Y., Shen, X., Xu, T., Yin, Y., Zhang, H., Ding, S., Zhao, Y., Zhang, Y., Guan, Y., et al. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.105721 · Cited by 36
NADPH oxidase 4 (NOX4) as a biomarker and therapeutic target in neurodegenerative diseases
Boonpraman, N., & Yi, S. S. (2023) · Neural Regeneration Research · doi:10.4103/1673-5374.390973 · Cited by 37
“…in the increased NOX activity repeatedly observed in the progression of AD, PD, and other neurodegenerative diseases (Bruce-Keller et al., 2011; Ansari and Scheff, 2011; Kim et al., 2017) in various affected brain regions such as the hippocampus, cortex, substantia nigra, and cerebellum.”
BackgroundChen, X.-H., Zhou, X. P., Yang, X., Zhou, Z., Lu, D., Tang, Y., Ling, Z., Zhou, L., & Feng, X. (2015) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-015-0235-1 · Cited by 35
Ibrahim, W. W., Ismail, H. M., Khattab, M. M., & Abdelkader, N. F. (2020) · Toxicology and Applied Pharmacology · doi:10.1016/j.taap.2020.115028 · Cited by 35
Izuo, N., Kume, T., Sato, M., Murakami, K., Irie, K., Izumi, Y., & Akaike, A. (2012) · ACS Chemical Neuroscience · doi:10.1021/cn300033k · Cited by 34
NOX-induced oxidative stress is a primary trigger of major neurodegenerative disorders
Zilberter, Y., Tabuena, D. R., & Zilberter, M. Y. (2023) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2023.102539 · Cited by 35
“Notably, NOX activity has been found to have a robust negative correlation with cognitive status in humans (Ansari and Scheff, 2011).”
Background(−)-Epicatechin mitigates high fat diet-induced neuroinflammation and altered behavior in mice
Kang, J., Wang, Z., & Oteiza, P. I. (2020) · Food & Function · doi:10.1039/d0fo00486c · Cited by 35
The Role of Beta-Adrenergic Receptor Blockers in Alzheimer’s Disease
Lương, K. V. Q., & Nguyễn, L. (2013) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/1533317513488924 · Cited by 32
“The NOX is also upregulated in the frontal and temporal cortices and contributes to AD progression.(124) The inhibition of NOX or the gene deletion of its functional p47 (phox: phagocyte oxidation) subunit promotes alternative and anti-inflammatory microglial activation during neuroinflammation.”
BackgroundLobine, D., Sadeer, N., Jugreet, S., Suroowan, S., Keenoo, B. S., Imran, M., Venugopala, K. N., Ibrahim, F. M., Zengin, G., & Mahomoodally, M. F. (2021) · Current Neuropharmacology · doi:10.2174/1570159x19666210412095251 · Cited by 32
“A direct association between cognitive impairment in AD patients and the increase of NOX activity has also been reported [36].”
BackgroundUnifying mechanism behind the onset of acquired epilepsy
Zilberter, Y., Popova, I. Y., & Zilberter, M. Y. (2021) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2021.11.009 · Cited by 32
Oxidative Stress, Neuroinflammation, and Neurodegeneration
Gao, H., Zhou, H., & Hong, J. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1071-7_5 · Cited by 30
“Brain tissues of patients with AD reveal increased mRNA transcripts of NOX1 and NOX3 as well as elevated expression and activity of NOX2 [ 39 – 41 ].”
BackgroundPepping, J. K., Vandanmagsar, B., Fernandez-Kim, S.-O., Zhang, J., Mynatt, R. L., & Bruce‐Keller, A. J. (2017) · PLoS ONE · doi:10.1371/journal.pone.0181500 · Cited by 29
Identification of New Targets and the Virtual Screening of Lignans against Alzheimer’s Disease
Maia, M. D. S., Rodrigues, G. C. S., de Sousa, N. F., Scotti, M. T., Scotti, L., & Mendonça, F. J. B. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/3098673 · Cited by 29
“[42, 43], molecules with molecular weights below 500Da, calculated log P (ClogP) values less than five, less than five hydrogen bond donors, no more than ten hydrogen bond acceptors, and ≤10 rotating bonds have excellent absorption and bioavailability.”
BackgroundPatrick, S., Corrigan, R. R., Grizzanti, J., Mey, M., Blair, J., Pallàs, M., Camins, A., Lee, H., & Casadesús, G. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180421 · Cited by 27
“As discussed previously, patients with MCI and AD exhibitdecreasedtotalantioxidantcapability[60]and increasedproductionofO 2 • – [80] which stimulates the amyloidogenic pathway [81].”
Zhou, Z., Wang, M., Huang, C., Li, Y., Gao, L., Zhu, Y., Ying, C., & Zhou, X. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.09.018 · Cited by 26
Glutamine Supplementation Prevents Chronic Stress-Induced Mild Cognitive Impairment
Baek, J. H., Jung, S., Son, H., Kang, J. S., & Kim, H. J. (2020) · Nutrients · doi:10.3390/nu12040910 · Cited by 24
Hashimoto, Y., Toyama, Y., Kusakari, S., Nawa, M., & Matsuoka, M. (2016) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.698092 · Cited by 26
Reddan, J. M., White, D., Macpherson, H., Scholey, A. B., & Pipingas, A. (2018) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2018.00049 · Cited by 29
“…may contribute to endothelial dysfunction, distorted smooth muscle growth as well as inflammation (Giordano and Visioli, 2014), and has been linked to an increased risk of MCI and AD, while also predicting Braak stage—a measure of AD pathology (BruceKeller et al., 2010; Ansari and Scheff, 2011).”
BackgroundKan, H., Hu, W., Wang, Y., Wu, W., Yin, Y., Liang, Y., Wang, C., Huang, D., & Li, W. (2015) · Molecular Medicine Reports · doi:10.3892/mmr.2015.3894 · Cited by 24
“Previous studies have reported a correlation between NOX activity and the progression of Alzheimer's disease, suggesting that increased NADPH oxidase activity may be one of the early events in the transition from normal cognition to dementia (18,40,41).”
InfluentialThe Hidden Notes of Redox Balance in Neurodegenerative Diseases
Piccirillo, S., Magi, S., Preziuso, A., Serfilippi, T., Cerqueni, G., Orciani, M., Amoroso, S., & Lariccia, V. (2022) · Antioxidants · doi:10.3390/antiox11081456 · Cited by 26
“Increased levels of NOX activity have been observed in the frontal and temporal cortex of individuals with (MCI), suggesting an involvement of this enzyme complex in the earliest stages of AD [154].”
BackgroundAnsari, M. A., Rao, M. S. R., & Al‐Jarallah, A. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2023.1273626 · Cited by 23
Kim, J., & Moon, J. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms252212299 · Cited by 26
“This process is further supported by findings that A β induces NOX2 activation in microglia, leading to the production of ROS and pro-inflammatory cytokines, which exacerbate synaptic loss, neuronal damage, and cognitive decline [24].”
Mizutani, H., Sato, Y., Yamazaki, M., Yoshizawa, T., Ando, Y., Ueda, M., & Yamagata, K. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23169027 · Cited by 22
“Increased NOX activity in the brain of patients with AD and those with mild cognitive impairment was reported [36,37].”
BackgroundYang, L., Zhou, H., Huang, L., Su, Y., Kong, L., Ji, P., Sun, R., Wang, C., Li, W., & Li, W. (2022) · International Immunopharmacology · doi:10.1016/j.intimp.2022.108972 · Cited by 23
Chronic stress alters the expression levels of longevity-related genes in the rat hippocampus
Sánchez-Hidalgo, A. C., Muñoz, M., Herrera, A. J., Espinosa‐Oliva, A. M., Stowell, R. D., Ayala, A., Machado, A., Venero, J. L., & de Pablos, R. M. (2016) · Neurochemistry International · doi:10.1016/j.neuint.2016.04.009 · Cited by 23
Gao, M., Kang, Y., Zhang, L., Li, H., Qu, C., Luan, X., Liu, L., & Zhang, S. (2020) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2020.4653 · Cited by 21
“The cytosolic subunit proteins were significantly elevated with the progression of Alzheimer's disease (40).”
BackgroundWalsh, K. P., Kuhn, T. B., & Bamburg, J. R. (2014) · Prion · doi:10.4161/pri.35504 · Cited by 21
Cooperation between neurovascular dysfunction and Aβ in Alzheimer’s disease
Wang, N., Yang, X., Zhao, Z., Liu, D., Wang, X., Tang, H., Zhong, C., Chen, X., Chen, W. K., & Meng, Q. (2023) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2023.1227493 · Cited by 22
Pallebage‐Gamarallage, M. M., Takechi, R., Lam, V., Elahy, M., & Mamo, J. C. L. (2015) · Critical Reviews in Clinical Laboratory Sciences · doi:10.3109/10408363.2015.1115820 · Cited by 20
Doğan, H. O., & Yıldız, Ö. K. (2019) · Journal of Trace Elements in Medicine and Biology · doi:10.1016/j.jtemb.2019.05.011 · Cited by 20
da Silva, P. R., Andrade, J., de Sousa, N. F., Portela, A. C. R., Pires, H. F. O., Remígio, M. C. R. B., Alves, D. D. N., de Andrade, H. H. N., Dias, A. L., Salvadori, M. G. D. S. S., et al. (2023) · Current Neuropharmacology · doi:10.2174/1570159x21666230221123059 · Cited by 19
Fu, Q., Gao, N., Yu, J., Ma, G., Du, Y., Wang, F., Su, Q., & Che, F. (2014) · Neurochemical Research · doi:10.1007/s11064-014-1313-3 · Cited by 18
“Brain tissue samples of AD patients reveal an elevation in NOX2 activity, and an upregulation and membrane translocation of cytosolic subunits of PHOX, which implies NOX2-associated oxidative damage in the pathogenesis of AD [10, 11].”
BackgroundThe Role of NOX4 in Parkinson’s Disease with Dementia
Choi, D., Choi, I.-A., Lee, C.-S., Yun, J. H., & Lee, J. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20030696 · Cited by 18
“Studies of postmortem brain tissues of AD patients demonstrated an upregulation of the p67phox, p47phox, and p40phox isoforms and an increase in NOX enzymatic activity [25].”
BackgroundInfluentialOxidative stress precedes mitochondrial dysfunction in gerbil brain after aluminum ingestion
Vucetic-Arsic, S., Radonjić, N. V., Jovanović, M., Selaković, V., Nikolić, T., Velimirović, M., Stojković, T., Milovanović, A., Milovanovic, J. P., & Petronijević, N. (2013) · Environmental Toxicology and Pharmacology · doi:10.1016/j.etap.2013.10.008 · Cited by 18
NOX2 in Alzheimer's and Parkinson's disease
Dustin, C. M., Shiva, S. S., Vazquez, A. L., Saeed, A., Pascoal, T. A., Cifuentes-Pagano, E., & Pagano, P. J. (2024) · Redox Biology · doi:10.1016/j.redox.2024.103433 · Cited by 19
Radbruch, H., Mothes, R., Bremer, D., Seifert, S., Köhler, R., Pohlan, J., Ostendorf, L., Günther, R., Leben, R., Stenzel, W., et al. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.00844 · Cited by 15
“In addition, there was a robust correlation between NOX subunit expression and the individual’s cognitive status (11).”
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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