ReviewToxicological sciences : an official journal of the Society of Toxicology2018
Environmental and Dietary Exposure to Copper and Its Cellular Mechanisms Linking to Alzheimer's Disease.
Review in Toxicological sciences : an official journal of the Society of Toxicology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed.
- Cu(OH)Particle and fibre toxicology · 2026Article
- From cooperation to collapse: the diet-microbiota-host gene triad in disease and aging.Frontiers in microbiomes · 2026Review
- Metal-Catalyzed Abiotic Cleavage of C═C Bonds for Effective Fluorescence Imaging of Cu(II) and Fe(III) in Living Systems.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Effects of Fisetin and Curcumin on Oxidative Damage Caused by Transition Metals in Neurodegenerative Diseases.Molecular neurobiology · 2025Review
- Copper, Iron, Cadmium, and Arsenic, All Generated in the Universe: Elucidating Their Environmental Impact Risk on Human Health Including Clinical Liver Injury.International journal of molecular sciences · 2024Review
- Environmental Toxins and Alzheimer's Disease: a Comprehensive Analysis of Pathogenic Mechanisms and Therapeutic Modulation.Molecular neurobiology · 2024Review
- Data-Driven Characterization of Genetic Variability in Disease Pathways and Pesticide-Induced Nervous System Disease in the United States Population.Environmental health perspectives · 2024Article
- Article
- Insights Into the Role of Copper in Neurodegenerative Diseases and the Therapeutic Potential of Natural Compounds.Current neuropharmacology · 2024Review
- Exposure to copper induces endoplasmic reticulum (ER) stress-mediated apoptosis in chicken (Gallus gallus) myocardium.Veterinary research communications · 2023Article
- Among Gerontogens, Heavy Metals Are a Class of Their Own: A Review of the Evidence for Cellular Senescence.Brain sciences · 2023Review
- A national survey of lead and other metal(loids) in residential drinking water in the United States.Journal of exposure science & environmental epidemiology · 2023Article
- miRNAs and Stem Cells as Promising Diagnostic and Therapeutic Targets for Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Copper sulfate induces clinico-hematological, oxidative stress, serum biochemical and histopathological changes in freshwater fish rohu (Frontiers in veterinary science · 2023Article
- Effect of Sublethal Copper Overload on CholesterolACS omega · 2022Article
- Is There a Connection between the Metabolism of Copper, Sulfur, and Molybdenum in Alzheimer's Disease? New Insights on Disease Etiology.International journal of molecular sciences · 2022Review
- Neuropathological and Cognitive Effects Induced by CuO-NPs in Rats and Trials for Prevention Using Pomegranate Juice.Neurochemical research · 2021Article
- 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
- Article
- Neurotoxicity in Marine Invertebrates: An Update.Biology · 2021Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Metals are commonly found in the environment, household, and workplaces in various forms, and a significant segment of the population is routinely exposed to the trace amount of metals from variety of sources. Exposure to metals, such as aluminum, lead, iron, and copper, from environment has long been debated as a potential environmental risk factor for Alzheimer's disease (AD) for decades, yet results from in vitro, in vivo, and human population remain controversial. In the case of copper, the neurotoxic mechanism of action was classically viewed as its strong affinity to amyloid-beta (Aβ) to help its aggregation and increase oxidative stress via Fenton reaction. Thus, it has been thought that accumulation of copper mediates neurotoxicity, and removing it from the brain prevents or reverse Aβ plaque burden. Recent evidence, however, suggests dyshomeostasis of copper and its valency in the body, instead of the accumulation and interaction with Aβ, are major determinants of its beneficial effects as an essential metal or its neurotoxic counterpart. This notion is also supported by the fact that genetic loss-of-function mutations on copper transporters lead to severe neurological symptoms. Along with its altered distribution, recent studies have also proposed novel mechanisms of copper neurotoxicity mediated by nonneuronal cell lineages in the brain, such as capillary endothelial cells, leading to development of AD neuropathology. This review covers recent findings of multifactorial toxic mechanisms of copper and discusses the risk of environmental exposure as a potential factor in accounting for the variability of AD incidence.
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