ArticleJournal of Alzheimer's disease : JAD2017
Diabetes and Alzheimer's Disease: Can Elevated Free Copper Predict the Risk of the Disease?
Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 43 citations in OpenAlex.
- Serum copper modulates cognitive function in diabetic patients via an HDL-C-mediated pathway: identification of a 25 µg/dL exploratory threshold.Diabetology & metabolic syndrome · 2025Article
- Exchangeable Copper Excess and Zinc Deficiency in the Serum of Patients with Colorectal Cancer.Biological trace element research · 2025Article
- The Role of Copper in Alzheimer's Disease Etiopathogenesis: An Updated Systematic Review.Toxics · 2024Review
- Associations between patterns of blood heavy metal exposure and health outcomes: insights from NHANES 2011-2016.BMC public health · 2024Article
- Sulfur-bridging the gap: investigating the electrochemistry of novel copper chelating agents for Alzheimer's disease applications.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2023Article
- Review
- 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
- Concentration and potential health risks of trace metals in warty crab (Eriphia verrucosa Forskal, 1775) from Southern Coasts of the Black Sea, Turkey.Environmental science and pollution research international · 2021Article
- Beneficial Impact of Semicarbazide-Sensitive Amine Oxidase Inhibition on the Potential Cytotoxicity of Creatine Supplementation in Type 2 Diabetes Mellitus.Molecules (Basel, Switzerland) · 2020Review
- Critical Review of Exposure and Effects: Implications for Setting Regulatory Health Criteria for Ingested Copper.Environmental management · 2020Review
- Overcoming Resistance to Therapies Targeting the MAPK Pathway in BRAF-Mutated Tumours.Journal of oncology · 2020Review
- A potent, selective, and orally bioavailable inhibitor of the protein-tyrosine phosphatase PTP1B improves insulin and leptin signaling in animal models.The Journal of biological chemistry · 2018Article
- Identification of Potential Therapeutic Targets in the Liver of Pioglitazone-Treated Type 2 Diabetes Sprague-Dawley Rats via Expression Profile Chip and iTRAQ Assay.Journal of diabetes research · 2018Article
- Thiol oxidase ability of copper ion is specifically retained upon chelation by aldose reductase.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2017Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDefective copper regulation, primarily referred to as chelatable redox active Cu(II), has been involved in the etiology of diabetes, and Alzheimer's disease (AD).
objectivesHowever, no study has determined levels of labile copper non-bound to ceruloplasmin (non-Cp Cu, also known as 'free' copper) in the blood of subjects with diabetes compared with that of AD patients.
methodsTo this aim, values of non-Cp Cu were measured in 25 Type 1 (T1D) and 31 Type 2 (T2D) subjects and in28 healthy controls, along with measurements of C-reactive protein, glycated hemoglobin A1c, cholesterol, and triglycerides. Non-Cp Cu levels were compared with those of an AD group previously studied.
resultsT2D subjects had significantly higher non-Cp Cu levels than Controls and T1D subjects (both p < 0.001 after adjusting for age, sex, and body mass index). A multinomial logistic model revealed that a one unit standard deviation increase of non-Cp Cu increased the relative risk of having T2D by 9.64 with respect to Controls (95% CI: 2.86-32.47). The comparison of non-Cp Cu levels in T2D with those of an AD population previously studied shows rising blood non-Cp Cu copper levels from Controls to T2D and AD.
conclusionThese results suggest the involvement of catalytically-active Cu(II) and glucose dysregulation in oxidative stress reactions leading to tissue damage in both diseases.
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