ArticleNeurobiology of aging2013
Inhibition of human high-affinity copper importer Ctr1 orthologous in the nervous system of Drosophila ameliorates Aβ42-induced Alzheimer's disease-like symptoms.
Article in Neurobiology of aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 49 citations in OpenAlex.
- Review
- The interactions of copper, glutamate, and cuproptosis: insights into brain health and Alzheimer's disease pathology.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Harnessing copper: Innovative approaches to combat neurodegenerative diseases and cancer (Review).International journal of molecular medicine · 2026Review
- Integrating cuproptosis and immunosenescence: A novel therapeutic strategy in cancer treatment.Biochemistry and biophysics reports · 2025Review
- Pharmacological mechanisms and therapeutic prospects of plant metabolites from traditional Chinese medicine in regulating programmed cell death in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Altered copper transport in oxidative stress-dependent brain endothelial barrier dysfunction associated with Alzheimer's disease.Vascular pharmacology · 2024Article
- Copper homeostasis and cuproptosis in central nervous system diseases.Cell death & disease · 2024Review
- Identification of cuproptosis-related genes in Alzheimer's disease based on bioinformatic analysis.European journal of medical research · 2024Article
- Challenges and Opportunities of Metal Chelation Therapy in Trace Metals Overload-Induced Alzheimer's Disease.Neurotoxicity research · 2023Review
- Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023Review
- Copper homeostasis and cuproptosis in health and disease.Signal transduction and targeted therapy · 2022Review
- Toxicities of amyloid-beta and tau protein are reciprocally enhanced in theNeural regeneration research · 2022Article
- Exposure of metal toxicity in Alzheimer's disease: An extensive review.Frontiers in pharmacology · 2022Review
- Redox-Active Metal Ions and Amyloid-Degrading Enzymes in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Molecular Mechanisms of Metal Toxicity in the Pathogenesis of Alzheimer's Disease.Molecular neurobiology · 2021Review
- Determination of Metal Content in Drosophila melanogaster During Metal Exposure.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.International journal of molecular sciences · 2020Review
- Genetic Dissection of Alzheimer's Disease UsingInternational journal of molecular sciences · 2020Review
- Copper trafficking in eukaryotic systems: current knowledge from experimental and computational efforts.Current opinion in structural biology · 2019Review
- Biometal Dyshomeostasis and Toxic Metal Accumulations in the Development of Alzheimer's Disease.Frontiers in molecular neuroscience · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
Disruption of copper homeostasis has been implicated in Alzheimer's disease (AD) during the last 2 decades; however, whether copper is a friend or a foe is controversial. Within a genetically tractable Drosophila AD model, we manipulated the expression of human high-affinity copper importer orthologous in Drosophila to explore the in vivo roles of copper ions in the development of AD. We found that inhibition of Ctr1C expression by RNAi in Aβ-expressing flies significantly reduced copper accumulation in the brains of the flies as well as ameliorating neurodegeneration, enhancing climbing ability, and prolonging lifespan. Interestingly, Ctr1C inhibition led to a significant increase in higher-molecular-weight Aβ42 forms in brain lysates, whereas it was accompanied by a trend of decreased expression of amyloid-β degradation proteases (including NEP1-3 and IDE) with age and reduced Cu-Aβ interaction-induced oxidative stress in Ctr1C RNAi flies. Similar results were obtained from inhibiting another copper importer Ctr1B and overexpressing a copper exporter DmATP7 in the nervous system of AD flies. These results imply that copper may play a causative role in developing AD, as either Aβ oligomers or aggregates were less toxic in a reduced copper environment or one with less copper binding. Early manipulation of brain copper uptake can have a great effect on Aβ pathology.
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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.