ArticleJournal of clinical biochemistry and nutrition2022
Crosstalk of copper and zinc in the pathogenesis of vascular dementia.
Article in Journal of clinical biochemistry and nutrition, 2022. 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, 13 citations in OpenAlex.
- Emerging role of copper in the pathophysiology of spinal cord injury.Neural regeneration research · 2026Article
- Identification of a Four-Gene Signature Based on Metal Metabolism for Alzheimer's Disease Diagnosis.Genes · 2025Article
- Investigating cerebral blood flow dysregulation and serum zinc correlation in 2-4 year-old children with autism spectrum disorder.European journal of medical research · 2025Article
- Cuproptosis Cell Death Molecular Events and Pathways to Liver Disease.Journal of inflammation research · 2025Review
- Imbalance of Plasma Copper and Zinc Levels and the Association Between the Cu/Zn Ratio and Lipid Peroxidation in Algerian Bipolar Patients.Biological trace element research · 2024Article
- Review
- Advances in reaction-based synthetic fluorescent probes for studying the role of zinc and copper ions in living systems.Journal of clinical biochemistry and nutrition · 2023Article
- Zinc in Human Health and Infectious Diseases.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Copper and zinc are essential for normal brain functions. Both are localized in presynaptic vesicles and are secreted into synaptic clefts during neuronal excitation. Despite their significance, excesses of copper and zinc are neurotoxic. In particular, excess zinc after transient global ischemia plays a central role in the ischemia-induced neurodegeneration and pathogenesis of vascular type senile dementia. We previously found that sub-lethal concentrations of copper remarkably exacerbated zinc-induced neurotoxicity, and we investigated the molecular pathways of copper-enhanced zinc-induced neurotoxicity. The endoplasmic reticulum stress pathway, the stress-activated protein kinases/c-Jun amino-terminal kinases pathway, and mitochondrial energy production failure were revealed to be involved in the neurodegenerative processes. Regarding the upstream factors of these pathways, we focused on copper-derived reactive oxygen species and the disruption of calcium homeostasis. Because excess copper and zinc may be present in the synaptic clefts during ischemia, it is possible that secreted copper and copper-induced reactive oxygen species may enhance zinc neurotoxicity and eventually contribute to the pathogenesis of vascular type senile dementia.
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Registered trials
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