ArticleNeurobiology of disease2011
Cognitive impairment in humanized APP×PS1 mice is linked to Aβ(1-42) and NOX activation.
Article in Neurobiology of disease, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
56 citing papers in PubMed, 94 citations in OpenAlex.
- Article
- Gut dysbiosis impacts estrogen levels in APP/PS1 transgenic female mice.Gut microbes · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Sex-Specific Effects of Anxiety on Cognition and Activity-Dependent Neural Networks: Insights From (Female) Mice and (Wo)men.Biological psychiatry · 2025Article
- NOX4-mediated astrocyte ferroptosis in Alzheimer's disease.Cell & bioscience · 2024Article
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Prolactin protects hippocampal neurons against H2O2-induced neurotoxicity by suppressing BAX and NOX4 via the NF-κB signaling pathway.PloS one · 2024Article
- Review
- Dendrimers and Derivatives as Multifunctional Nanotherapeutics for Alzheimer's Disease.Pharmaceutics · 2023Review
- Oxidative Stress in Brain in Amnestic Mild Cognitive Impairment.Antioxidants (Basel, Switzerland) · 2023Review
- Fasting-mimicking diet cycles reduce neuroinflammation to attenuate cognitive decline in Alzheimer's models.Cell reports · 2022Article
- Repurposed anti-cancer epidermal growth factor receptor inhibitors: mechanisms of neuroprotective effects in Alzheimer's disease.Neural regeneration research · 2022Review
- SIRT7 Deficiency Protects against AβInternational journal of molecular sciences · 2022Article
- Necrostatin-1 Relieves Learning and Memory Deficits in a Zebrafish Model of Alzheimer's Disease Induced by Aluminum.Neurotoxicity research · 2022Article
- Implication of type 4 NADPH oxidase (NOX4) in tauopathy.Redox biology · 2022Article
- Effect of Selenium Treatment on Central Insulin Sensitivity: A Proteomic Analysis in β-Amyloid Precursor Protein/Presenilin-1 Transgenic Mice.Frontiers in molecular neuroscience · 2022Article
- A nexus of miR-1271, PAX4 and ALK/RYK influences the cytoskeletal architectures in Alzheimer's Disease and Type 2 Diabetes.The Biochemical journal · 2021Article
- NADPH Oxidases (NOX): An Overview from Discovery, Molecular Mechanisms to Physiology and Pathology.Antioxidants (Basel, Switzerland) · 2021Review
- miR-204-3p/Nox4 Mediates Memory Deficits in a Mouse Model of Alzheimer's Disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Nitric Oxide Pathways in Neurovascular Coupling Under Normal and Stress Conditions in the Brain: Strategies to Rescue Aberrant Coupling and Improve Cerebral Blood Flow.Frontiers in physiology · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Cognitive impairment in Alzheimer's disease (AD) is strongly associated with both extensive deposition of amyloid β peptides and oxidative stress, but the exact role of these indices in the development of dementia is not clear. This study was designed to determine the relationship between cognitive impairment, activation of the free radical producing enzyme NADPH oxidase (NOX), and progressive changes in Aβ deposition and solubility in humanized APP×PS1 knock-in mice of increasing age. Data show that cognitive performance and expression of key synaptic proteins were progressively decreased in aging APP×PS1 mice. Likewise, NOX activity and expression of the specific NOX subunit NOX4 were significantly increased in APP×PS1 mice in an age-dependent manner, and NOX activity and cognitive impairment shared a significant linear relationship. Data further show that age-dependent increases in Aβ(1-42) had a significant linear relationship with both NOX activity and cognitive performance in APP×PS1 knock-in mice. Collectively, these data show that NOX expression and activity are significantly upregulated with age in this humanized model of Aβ pathogenesis, and suggest that NOX-associated redox pathways are intimately linked to both the loss of cognitive function and the deposition of Aβ(1-42).
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.