ArticleInternational journal of molecular sciences2012
Alzheimer's disease-associated neurotoxic peptide amyloid-β impairs base excision repair in human neuroblastoma cells.
Article in International journal of molecular sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- Activated or Impaired: An Overview of DNA Repair in Neurodegenerative Diseases.Aging and disease · 2022Article
- Impairment of Base Excision Repair in Dermal Fibroblasts Isolated From Nevoid Basal Cell Carcinoma Patients.Frontiers in oncology · 2020Article
- Xeroderma Pigmentosum C (XPC) Mutations in Primary Fibroblasts Impair Base Excision Repair Pathway and Increase Oxidative DNA Damage.Frontiers in genetics · 2020Article
- Activation of Nrf2 Pathway Contributes to Neuroprotection by the Dietary Flavonoid Tiliroside.Molecular neurobiology · 2018Article
- Age-Dependent Protective Effect of Selenium against UVA Irradiation in Primary Human Keratinocytes and the Associated DNA Repair Signature.Oxidative medicine and cellular longevity · 2018Article
- Genome instability in Alzheimer disease.Mechanisms of ageing and development · 2017Review
- Combination of Aβ Secretion and Oxidative Stress in an Alzheimer-Like Cell Line Leads to the Over-Expression of the Nucleotide Excision Repair Proteins DDB2 and XPC.International journal of molecular sciences · 2015Article
- DNA polymerase β deficiency leads to neurodegeneration and exacerbates Alzheimer disease phenotypes.Nucleic acids research · 2015Article
- The extreme variety of genotoxic response to benzo[a]pyrene in three different human cell lines from three different organs.PloS one · 2013Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the leading cause of dementia in developed countries. It is characterized by two major pathological hallmarks, one of which is the extracellular aggregation of the neurotoxic peptide amyloid-β (Aβ), which is known to generate oxidative stress. In this study, we showed that the presence of Aβ in a neuroblastoma cell line led to an increase in both nuclear and mitochondrial DNA damage. Unexpectedly, a concomitant decrease in basal level of base excision repair, a major route for repairing oxidative DNA damage, was observed at the levels of both gene expression and protein activity. Moreover, the addition of copper sulfate or hydrogen peroxide, used to mimic the oxidative stress observed in AD-affected brains, potentiates Aβ-mediated perturbation of DNA damage/repair systems in the "Aβ cell line". Taken together, these findings indicate that Aβ could act as double-edged sword by both increasing oxidative nuclear/mitochondrial damage and preventing its repair. The synergistic effects of increased ROS production, accumulated DNA damage and impaired DNA repair could participate in, and partly explain, the massive loss of neurons observed in Alzheimer's disease since both oxidative stress and DNA damage can trigger apoptosis.
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