Redox cycling of copper-amyloid β 1-16 peptide complexes is highly dependent on the coordination mode.

Copper (Cu)-amyloid β (Aβ) interactions play a role in the etiology of Alzheimer's disease. This work presents a spectroscopic and electrochemical study of two physiologically relevant Aβ-Cu(II) complexes, as a function of pH and relative Cu-Aβ(1-16) concentrations. Our results reveal that these coordination modes display distinct redox behaviors and provide experimental evidence for the existence of an intermediate Cu(I) species. A mechanism for the redox cycling of these complexes is proposed, providing further insight into the redox relevance of Aβ-Cu interactions.