ArticleInternational journal of Alzheimer's disease2013
Decreased copper in Alzheimer's disease brain is predominantly in the soluble extractable fraction.
Article in International journal of Alzheimer's disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
The trial behind it
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Who cites it
30 citing papers in PubMed, 64 citations in OpenAlex.
- Distinct Effects of Copper Ionophores on Intracellular Copper and Cell Viability in Wild-Type and CTR1-Deficient SH-SY5Y Cells.ACS omega · 2026Article
- Metallothionein and neurodegenerative diseases.Neural regeneration research · 2026Article
- Decreased metallothionein-3 expression in the human spinal cord is a common feature of amyotrophic lateral sclerosis and multiple sclerosis.Scientific reports · 2026Article
- Harnessing copper: Innovative approaches to combat neurodegenerative diseases and cancer (Review).International journal of molecular medicine · 2026Review
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- A primer on copper biology in the brain.Neurobiology of disease · 2025Review
- From copper homeostasis to cuproptosis: a new perspective on CNS immune regulation and neurodegenerative diseases.Frontiers in neurology · 2025Review
- The role of intracellular and extracellular copper compartmentalization in Alzheimer's disease pathology and its implications for diagnosis and therapy.Frontiers in neuroscience · 2025Review
- Naringin and Naringenin: Potential Multi-Target Agents for Alzheimer's Disease.Current medical science · 2024Review
- Restoring cellular copper homeostasis in Alzheimer disease: a novel peptide shuttle is internalized by an ATP-dependent endocytosis pathway involving Rab5- and Rab14-endosomes.Frontiers in molecular biosciences · 2024Article
- Distribution of Iron, Copper, Zinc and Cadmium in Glia, Their Influence on Glial Cells and Relationship with Neurodegenerative Diseases.Brain sciences · 2023Review
- Biometals in Alzheimer disease: emerging therapeutic and diagnostic potential of molybdenum and iodine.Journal of translational medicine · 2023Review
- Copper homeostasis and the ubiquitin proteasome system.Metallomics : integrated biometal science · 2023Review
- Revisiting the Role of Vitamins and Minerals in Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Brain copper may protect from cognitive decline and Alzheimer's disease pathology: a community-based study.Molecular psychiatry · 2022Article
- An Adequate Supply of Bis(ethylmaltolato)oxidovanadium(IV) Remarkably Reversed the Pathological Hallmarks of Alzheimer's Disease in Triple-Transgenic Middle-Aged Mice.Biological trace element research · 2022Article
- Copper Toxicity Links to Pathogenesis of Alzheimer's Disease and Therapeutics Approaches.International journal of molecular sciences · 2020Review
- Article
- Current understanding of metal ions in the pathogenesis of Alzheimer's disease.Translational neurodegeneration · 2020Review
- Copper-Induced Upregulation of MicroRNAs Directs the Suppression of Endothelial LRP1 in Alzheimer's Disease Model.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the leading cause of dementia and represents a significant burden on the global economy and society. The role of transition metals, in particular copper (Cu), in AD has become of significant interest due to the dyshomeostasis of these essential elements, which can impart profound effects on cell viability and neuronal function. We tested the hypothesis that there is a systemic perturbation in Cu compartmentalization in AD, within the brain as well as in the periphery, specifically within erythrocytes. Our results showed that the previously reported decrease in Cu within the human frontal cortex was confined to the soluble (P < 0.05) and total homogenate (P < 0.05) fractions. No differences were observed in Cu concentration in erythrocytes. Our data indicate that there is a brain specific alteration in Cu levels in AD localized to the soluble extracted material, which is not reflected in erythrocytes. Further studies using metalloproteomics approaches will be able to elucidate the metabolic mechanism(s) that results in the decreased brain Cu levels during the progression of AD.
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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.