ReviewFrontiers in neuroscience2025
The role of intracellular and extracellular copper compartmentalization in Alzheimer's disease pathology and its implications for diagnosis and therapy.
Review in Frontiers in neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Advances in ferroptosis and cuproptosis: implications for spinal cord injury.Molecular biology reports · 2026Review
- Identification of Alzheimer's disease subtypes and biomarkers from human multi-omics data using subspace merging algorithm.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- β-Alanine Is an Unexploited Neurotransmitter in the Pathogenesis and Treatment of Alzheimer's Disease.NeuroSci · 2026Review
- Tolcapone Interferes With Key Pathological Features in Alzheimer's Disease.Bioinorganic chemistry and applications · 2026Article
- 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
- A Pilot Study on Blood Concentration of β-Amyloid (40 and 42) and Phospho-Tau 181 in Horses.Veterinary sciences · 2025Article
- CLSI Validation of Exchangeable Copper Determination in Serum by ICP-MS: A Focus on Alzheimer's Disease and Wilson Disease.Biomolecules · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper is a trace element indispensable for cellular physiology, integral to cellular redox balance, and a constituent of enzyme active sites, thereby playing a pivotal role in cellular physiological function. Concerning the pathogenesis of Alzheimer's disease (AD), the homeostatic balance of copper is perturbed both intracellularly and extracellularly. The copper-amyloid precursor protein (APP) complex facilitates the efflux of copper from cells, leading to intracellular copper depletion. Concurrently, extracellular copper associates with amyloid-beta (Aβ) plaques, precipitating copper-enriched Aβ deposition and augmenting reactive oxygen species (ROS) in the brain tissue, which finally culminates in oxidative brain damage. The interaction between copper and APP enhances the α-secretase pathway of APP processing while suppressing the β-secretase pathway, resulting in an increased production of soluble APP (sAPP), which contributes to neuroinflammation in the brain tissue. Utilizing the affinity of copper for Aβ plaques, the application of chelating agents to sequester copper within the brain can mitigate neurodegeneration associated with AD pathology. Furthermore, the use of metal imaging techniques to detect copper in the brain offers a potential diagnostic tool for the early identification 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 Socratic graph.