ArticleNeuromolecular medicine2013
ATP7B variants as modulators of copper dyshomeostasis in Alzheimer's disease.
Article in Neuromolecular medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 68 citations in OpenAlex.
- Review
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- Copper homeostasis and cuproptosis: implications for neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- The Role of Copper in Alzheimer's Disease Etiopathogenesis: An Updated Systematic Review.Toxics · 2024Review
- Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.International journal of molecular sciences · 2020Review
- Agricultural Use of Copper and Its Link to Alzheimer's Disease.Biomolecules · 2020Review
- Copper accumulation and the effect of chelation treatment on cerebral amyloid angiopathy compared to parenchymal amyloid plaques.Metallomics : integrated biometal science · 2020Article
- Single nucleotide polymorphisms in the human ATP7B gene modify the properties of the ATP7B protein.Metallomics : integrated biometal science · 2019Article
- Avoiding Alzheimer's disease: The important causative role of divalent copper ingestion.Experimental biology and medicine (Maywood, N.J.) · 2019Review
- A case of a mild Wolfram Syndrome with concomitantCellR4-- repair, replacement, regeneration, & reprogramming · 2019Article
- Environmental and Dietary Exposure to Copper and Its Cellular Mechanisms Linking to Alzheimer's Disease.Toxicological sciences : an official journal of the Society of Toxicology · 2018Review
- Human copper transporter ATP7B (Wilson disease protein) forms stable dimersThe Journal of biological chemistry · 2017Article
- Wilson disease: At the crossroads between genetics and epigenetics-A review of the evidence.Liver research (Beijing, China) · 2017Article
- Identification of two novel mutations in the ATP7B gene that cause Wilson's disease.World journal of pediatrics : WJP · 2017Article
- Serum Copper, Zinc, and Iron Levels in Patients with Alzheimer's Disease: A Meta-Analysis of Case-Control Studies.Frontiers in aging neuroscience · 2017Article
- Role of Copper in the Onset of Alzheimer's Disease Compared to Other Metals.Frontiers in aging neuroscience · 2017Review
- Non-Ceruloplasmin Copper Distincts Subtypes in Alzheimer's Disease: a Genetic Study of ATP7B Frequency.Molecular neurobiology · 2017Article
- Reply to B. Meunier's Letter to the Editor Re: Brewer G. J.; Nutrients 2015, 7, 10053-10064.Nutrients · 2016Article
- Review
- Novel mutations of the ATP7B gene in Han Chinese families with pre-symptomatic Wilson's disease.World journal of pediatrics : WJP · 2015Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To understand the role of the key copper-regulating gene, ATP7B, in copper dyshomeostasis associated with Alzheimer's disease (AD), we analyzed the serum levels of copper, ceruloplasmin and 'free' (i.e., non-ceruloplasmin bound) copper in 399 patients with AD and 303 elderly healthy controls. We also performed analyses of informative variants of ATP7B. AD patients had higher levels of copper and free copper than controls. Individuals with free copper levels higher than 1.6 μmol/L (the upper value of the normal reference range) were more frequent among cases (p < 0.001). Among these individuals, those who were carriers of the ATP7B variants accounted for a large proportion of the free copper levels, specifically in the AD group (p < 0.01). Our results suggest the existence of a 'copper dysfunction' phenotype of sporadic AD which has a genetic basis. They also suggest that free copper is a risk factor for this disorder, modulating additional pathways leading to the disease cascade.
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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.