ArticleBrain sciences2025
Downregulation of Parahippocampal Copper Chaperone for Superoxide Dismutase in Alzheimer's Disease.
Article in Brain sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Genomic structural variations distinguishing archaic and modern humans are associated with neurodevelopment.iScience · 2026Article
- From copper transport to cuproptosis: emerging therapeutic targets in cardiovascular disease.Molecular and cellular biochemistry · 2026Review
- Single-cell RNA sequencing reveals NFATc1-mediated regulatory mechanisms of vascular smooth muscle cell osteogenic transformation in the osteosarcoma microenvironment.Discover oncology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
BACKGROUND/
objectivesProper regulation of copper is essential for maintaining neuronal stability and is facilitated by several chaperone proteins, protecting cells from oxidative damage that would otherwise be caused by improperly regulated copper ions. Oxidative stress, resulting from such dysregulation, is hypothesized to play a significant role in the pathogenesis of Alzheimer's disease (AD).
methodsIn this study, we evaluated the concentrations of the copper chaperones CCS, DCTN4, and ATOX1 in control and AD cases via Western blotting and ELISA, and quantified the copper concentrations in fractionated neurons using ICP-MS.
resultsOur findings reveal a significant reduction in CCS levels in AD cases (
conclusionsThese results suggest a strong association between reduced CCS levels and AD pathology, highlighting a potential role for CCS in the redistribution of copper ions within neurons. This redistribution may contribute to oxidative stress and neuronal dysfunction, offering new insights into the mechanisms underlying AD pathogenesis.
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Registered trials
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