ArticleFrontiers in aging neuroscience2014
Alzheimer's disease causation by copper toxicity and treatment with zinc.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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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Who cites it
40 citing papers in PubMed, 70 citations in OpenAlex.
- Copper Homeostasis and Cuproptosis in Neurological Disorders.Drug design, development and therapy · 2026Review
- Copper homeostasis and cuproptosis in Alzheimer's disease (Review).International journal of molecular medicine · 2025Review
- Chronic Copper Overload Triggers Inflammation in Mesenteric PVAT Alongside Changes in Renin-Angiotensin System-Related Pathways.Nutrients · 2025Article
- Association between Copper Exposure and Cognitive Function: A Cross-Sectional Study in a County, Guangxi, China.Biological trace element research · 2025Article
- Copper homeostasis and pregnancy complications: a comprehensive review.Journal of assisted reproduction and genetics · 2025Review
- Neurotoxic Effect of Myricitrin in Copper-Induced Oxidative Stress Is Mediated by Increased Intracellular CaAntioxidants (Basel, Switzerland) · 2025Article
- Sodium Thiosulfate: An Innovative Multi-Target Repurposed Treatment Strategy for Late-Onset Alzheimer's Disease.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Inflammation in Metal-Induced Neurological Disorders and Neurodegenerative Diseases.Biological trace element research · 2024Review
- Preparation and Characterization of Zn(II)-Stabilized AβACS chemical neuroscience · 2024Article
- Cerebrospinal fluid efflux through dynamic paracellular pores on venules as a missing piece of the brain drainage system.Exploration (Beijing, China) · 2024Article
- MAD-microbial (origin of) Alzheimer's disease hypothesis: from infection and the antimicrobial response to disruption of key copper-based systems.Frontiers in neuroscience · 2024Review
- Metabolomic changes in tear fluid following zinc biofortification in the BiZiFED nutritional study: a feasibility study.Frontiers in molecular biosciences · 2024Article
- Metals in Alzheimer's Disease.Biomedicines · 2023Review
- Dietary Intake Levels of Iron, Copper, Zinc, and Manganese in Relation to Cognitive Function: A Cross-Sectional Study.Nutrients · 2023Article
- A Review of the Role of Curcumin in Metal Induced Toxicity.Antioxidants (Basel, Switzerland) · 2023Review
- Non-Enzymatic Antioxidants against Alzheimer's Disease: Prevention, Diagnosis and Therapy.Antioxidants (Basel, Switzerland) · 2023Review
- Alternative Pharmacological Strategies for the Treatment of Alzheimer's Disease: Focus on Neuromodulator Function.Biomedicines · 2022Review
- Article
- The Associations of Dietary Copper With Cognitive Outcomes.American journal of epidemiology · 2022Article
- Curcumin and Nano-Curcumin Mitigate Copper Neurotoxicity by Modulating Oxidative Stress, Inflammation, and Akt/GSK-3β Signaling.Molecules (Basel, Switzerland) · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Evidence will be presented that the Alzheimer's disease (AD) epidemic is new, the disease being very rare in the 1900s. The incidence is increasing rapidly, but only in developed countries. We postulate that the new emerging environmental factor partially causal of the AD epidemic is ingestion of inorganic copper from drinking water and taking supplement pills, along with a high fat diet. Inorganic copper can be partially directly absorbed and elevate the serum free copper pool. The Squitti group has shown that serum free copper is elevated in AD, correlates with cognition, and predicts cognition loss. Thus, our inorganic copper hypothesis fits well with the Squitti group data. We have also shown that AD patients are zinc deficient compared to age-matched controls. Because zinc is a neuronal protective factor, we postulate that zinc deficiency may also be partially causative of AD. We carried out a small 6 month double blind study of a new zinc formulation and found that in patients age 70 and over, it protected against cognition loss. Zinc therapy also significantly reduced serum free copper in AD patients, so efficacy may come from restoring normal zinc levels, or from lowering serum free copper, or from both.
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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.