ArticlePloS one2017
Oxidative stress affects processing of amyloid precursor protein in vascular endothelial cells.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- A quantitative meta-analysis of vitamin C in the pathophysiology of Alzheimer's disease.Frontiers in aging neuroscience · 2022Pooled it
- Mapping the Polar Neuro-Interactome ofLife (Basel, Switzerland) · 2026Article
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Elucidating molecular pathogenesis and developing targeted therapeutic interventions for cerebrovascular endothelial cell-mediated vascular dementia.Frontiers in aging neuroscience · 2025Review
- Targeting vascular dementia: Molecular docking and dynamics of natural ligands against neuroprotective proteins.PloS one · 2025Article
- From Inhalation to Neurodegeneration: Air Pollution as a Modifiable Risk Factor for Alzheimer's Disease.International journal of molecular sciences · 2024Review
- PHPB ameliorates memory deficits and reduces oxidative injury in Alzheimer's disease mouse model by activating Nrf2 signaling pathway.Acta pharmacologica Sinica · 2024Article
- The role of PI3K signaling pathway in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Endogenous and Exogenous Regulation of Redox Homeostasis in Retinal Pigment Epithelium Cells: An Updated Antioxidant Perspective.International journal of molecular sciences · 2023Review
- Oxidative Stress and Aging as Risk Factors for Alzheimer's Disease and Parkinson's Disease: The Role of the Antioxidant Melatonin.International journal of molecular sciences · 2023Review
- Amyloid β-Peptide Causes the Permanent Activation of CaMKIIα through Its Oxidation.International journal of molecular sciences · 2022Article
- Review
- Article
- Alzheimer Disease: Recent Updates on Apolipoprotein E and Gut Microbiome Mediation of Oxidative Stress, and Prospective Interventional Agents.Aging and disease · 2022Review
- mTOR in Alzheimer disease and its earlier stages: Links to oxidative damage in the progression of this dementing disorder.Free radical biology & medicine · 2021Review
- A Review on Potential Footprints of Ferulic Acid for Treatment of Neurological Disorders.Neurochemical research · 2021Review
- Premature Senescence and Increased Oxidative Stress in the Thymus of Down Syndrome Patients.Frontiers in immunology · 2021Article
- Circadian Rhythm Disruption and Alzheimer's Disease: The Dynamics of a Vicious Cycle.Current neuropharmacology · 2021Article
- Inborn Errors of Adaptive Immunity in Down Syndrome.Journal of clinical immunology · 2020Review
- MiR-539-5p Decreases amyloid β-protein production, hyperphosphorylation of Tau and Memory Impairment by Regulating PI3K/Akt/GSK-3β Pathways in APP/PS1 Double Transgenic Mice.Neurotoxicity research · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundOxidative stress is thought to be a key player in the pathogenesis of neurodegenerative dementia, including Alzheimer's disease (AD). It has been assumed that oxidative stress contributes to the ß-amyloid deposition in cerebral blood vessels.
methodsIn order to prove this hypothesis, we examined the effect of oxidative stress on the processing of amyloid precursor protein (APP) in primary endothelial cells (EC) derived from cerebral cortical tissue of transgenic Tg2576 mice. Following exposure of EC by 1 μM hydrogen peroxide for up to 48 hours, formation and secretion of APP cleavage products sAPPα and sAPPß into the culture medium as well as the expression of endothelial APP were assessed.
resultsOxidative stress resulted in enhanced secretion of sAPPß into the culture medium as compared to controls (absence of hydrogen peroxide), which was accompanied by an increased APP expression, induction of VEGF synthesis, nitric oxide and oxygen free radicals productions, and differential changes of endothelial phospo-p42/44 MAPK expression.
conclusionThe data suggest that oxidative stress may represent a major risk factor in causing Aß deposition in the brain vascular system by initiating the amyloidogenic route of endothelial APP processing. The enhanced β-secretase activity following oxidative stress exposure, possibly promoted by phosphorylation of p42/44 MAPK.
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Registered trials
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