ReviewJournal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry2010
Copper in the brain and Alzheimer's disease.
Review in Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 487 citations in OpenAlex.
- Environmental risk factors for dementia: a systematic review.BMC geriatrics · 2016Pooled it
- Simultaneous Imaging of CuAngewandte Chemie (International ed. in English) · 2026Article
- Diagnosis and Potential Therapy of Brain Diseases UsingCurrent medicinal chemistry · 2026Article
- Alzheimer's disease diagnosis based on gene selection and cross-tissue validation.Frontiers in genetics · 2026Article
- Melatonin Supplementation in Alzheimer's disease: The Potential Role in Neurogenesis.Molecular neurobiology · 2025Review
- Navigating the landscape of protein folding and proteostasis: from molecular chaperones to therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Dual Metal Ion Sensing by an Azo Compound Derived from Thiazolo[3,2-a] Indole: A Selective and Sensitive Approach.Journal of fluorescence · 2025Article
- Simultaneous ratiometric fluorescence determination and removal of copper ions by a magnetic nanocomposite.Scientific reports · 2025Article
- Melatonin-A Powerful Antioxidant in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Integrating network pharmacology and in vivo study to explore the anti-Alzheimer's potential of3 Biotech · 2025Article
- A Review on Pyrazolines as Colorimetric Fluorescent Chemosensors for CuJournal of fluorescence · 2025Review
- Melatonin: A potential nighttime guardian against Alzheimer's.Molecular psychiatry · 2025Review
- Rings of Power: Controlling SOD Mimic Activity by the Addition of Pyridine Rings within the Pyridinophane Scaffold.Inorganic chemistry · 2024Article
- Recent Advances in Targeting Transition Metals (Copper, Iron, and Zinc) in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Computational evaluation of the oxidation of superoxide to molecular dioxygen mediated by NNNN-tetradentate copper complexes.RSC advances · 2024Article
- Pyrene-acylhydrazone-based Turn-on Fluorescent Probe for Highly Sensitive Detection CuJournal of fluorescence · 2024Article
- Article
- Dual-channel fluorescent sensor for rapid CuHeliyon · 2024Article
- Thermodynamic Studies of Complexes in Cu(II)/Uridine-5'-Diphosphoglucuronic Acid System.Molecules (Basel, Switzerland) · 2024Article
- A CuAnalytical sciences : the international journal of the Japan Society for Analytical Chemistry · 2024Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common form of neurodegenerative disease. The brain is particularly vulnerable to oxidative damage induced by unregulated redox-active metals such as copper and iron, and the brains of AD patients display evidence of metal dyshomeostasis and increased oxidative stress. The colocalisation of copper and amyloid beta (Abeta) in the glutamatergic synapse during NMDA-receptor-mediated neurotransmission provides a microenvironment favouring the abnormal interaction of redox-potent Abeta with copper under conditions of copper dysregulation thought to prevail in the AD brain, resulting in the formation of neurotoxic soluble Abeta oligomers. Interactions between Abeta oligomers and copper can further promote the aggregation of Abeta, which is the core component of extracellular amyloid plaques, a central pathological hallmark of AD. Copper dysregulation is also implicated in the hyperphosphorylation and aggregation of tau, the main component of neurofibrillary tangles, which is also a defining pathological hallmark of AD. Therefore, tight regulation of neuronal copper homeostasis is essential to the integrity of normal brain functions. Therapeutic strategies targeting interactions between Abeta, tau and metals to restore copper and metal homeostasis are discussed.
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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.