ArticlePloS one2013
Mild oxidative stress induces redistribution of BACE1 in non-apoptotic conditions and promotes the amyloidogenic processing of Alzheimer's disease amyloid precursor protein.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Smoking and increased Alzheimer's disease risk: a review of potential mechanisms.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2014Pooled it
- Enterogenic dementia: defining the gut-brain axis and the role of inflammatory bowel disease in cognitive impairment.Inflammopharmacology · 2025Review
- RhoA/ROCK/GSK3β Signaling: A Keystone in Understanding Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Design,Frontiers in pharmacology · 2023Article
- Melatonin as a Harmonizing Factor of Circadian Rhythms, Neuronal Cell Cycle and Neurogenesis: Additional Arguments for Its Therapeutic Use in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Pharmaceutical Potential of Casein-Derived Tripeptide Met-Lys-Pro: Improvement in Cognitive Impairments and Suppression of Inflammation in APP/PS1 Mice.Journal of Alzheimer's disease : JAD · 2022Article
- DNA Damage Increases Secreted Aβ40 and Aβ42 in Neuronal Progenitor Cells: Relevance to Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2022Article
- Lipid Peroxidation Induced ApoE Receptor-Ligand Disruption as a Unifying Hypothesis Underlying Sporadic Alzheimer's Disease in Humans.Journal of Alzheimer's disease : JAD · 2022Article
- Environmental exposures and the etiopathogenesis of Alzheimer's disease: The potential role of BACE1 as a critical neurotoxic target.Journal of biochemical and molecular toxicology · 2021Review
- Neuroprotective Potential of Verbascoside Isolated fromAntioxidants (Basel, Switzerland) · 2020Article
- Traffic-related air pollutants (TRAP-PM) promote neuronal amyloidogenesis through oxidative damage to lipid rafts.Free radical biology & medicine · 2020Article
- Serum beta-secretase 1 (BACE1) activity as candidate biomarker for late-onset Alzheimer's disease.GeroScience · 2020Article
- Decoding the Role of Platelets and Related MicroRNAs in Aging and Neurodegenerative Disorders.Frontiers in aging neuroscience · 2019Review
- Apolipoprotein D Upregulation in Alzheimer's Disease but Not Frontotemporal Dementia.Journal of molecular neuroscience : MN · 2019Article
- Molecular Mechanisms and Genetics of Oxidative Stress in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Review
- Hippocampal Proteomic Analysis Reveals Distinct Pathway Deregulation Profiles at Early and Late Stages in a Rat Model of Alzheimer's-Like Amyloid Pathology.Molecular neurobiology · 2018Article
- Comparative Evaluation of the Antioxidant and Anti-Alzheimer's Disease Potential of Coumestrol and Puerarol Isolated from Pueraria lobata Using Molecular Modeling Studies.Molecules (Basel, Switzerland) · 2018Article
- Neuroprotective Effects of Phenolic and Carboxylic Acids on Oxidative Stress-Induced Toxicity in Human Neuroblastoma SH-SY5Y Cells.Neurochemical research · 2018Article
- HIV Protease Inhibitors Alter Amyloid Precursor Protein Processing via β-Site Amyloid Precursor Protein Cleaving Enzyme-1 Translational Up-Regulation.The American journal of pathology · 2017Article
- α-Synuclein increases β-amyloid secretion by promoting β-/γ-secretase processing of APP.PloS one · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
BACE1 is responsible for β-secretase cleavage of the amyloid precursor protein (APP), which represents the first step in the production of amyloid β (Aβ) peptides. Previous reports, by us and others, have indicated that the levels of BACE1 protein and activity are increased in the brain cortex of patients with Alzheimer's disease (AD). The association between oxidative stress (OS) and AD has prompted investigations that support the potentiation of BACE1 expression and enzymatic activity by OS. Here, we have established conditions to analyse the effects of mild, non-lethal OS on BACE1 in primary neuronal cultures, independently from apoptotic mechanisms that were shown to impair BACE1 turnover. Six-hour treatment of mouse primary cortical cells with 10-40 µM hydrogen peroxide did not significantly compromise cell viability but it did produce mild oxidative stress (mOS), as shown by the increased levels of reactive radical species and activation of p38 stress kinase. The endogenous levels of BACE1 mRNA and protein were not significantly altered in these conditions, whereas a toxic H2O2 concentration (100 µM) caused an increase in BACE1 protein levels. Notably, mOS conditions resulted in increased levels of the BACE1 C-terminal cleavage product of APP, β-CTF. Subcellular fractionation techniques showed that mOS caused a major rearrangement of BACE1 localization from light to denser fractions, resulting in an increased distribution of BACE1 in fractions containing APP and markers for trans-Golgi network and early endosomes. Collectively, these data demonstrate that mOS does not modify BACE1 expression but alters BACE1 subcellular compartmentalization to favour the amyloidogenic processing of APP, and thus offer new insight in the early molecular events of AD pathogenesis.
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