Research shows that copper-chelating ligands exhibit antioxidant properties in neurodegenerative models, suggesting new treatment avenues.
Oxidative stress, driven by excess reactive oxygen species (ROS), is a key factor in the progression of neurodegenerative diseases like Alzheimer’s disease (AD). In this context, copper dysregulation can also contribute to this imbalance, being responsible for enhanced ROS production, so that copper scavenging has been investigated as a possible therapeutic strategy. This study investigates the behavior of two isostructural ligands, featuring an N3O donor set, that effectively chelate Cu(II) in aqueous solution. Interestingly, their resulting mono- or dinuclear copper complexes feature a coordination environment suitable to foster antioxidant activity. By transforming copper’s oxidant potential into antioxidant action, these systems may reduce copper-induced oxidative damage. The work examines the pH-dependent metal-binding behavior of the ligands, the catalytic properties of the resulting complexes under physiological conditions, and their ability to inhibit β-amyloid peptide aggregation.
No takes yet. Share an insight, caveat, or question.
Zonzin et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: