Redox behaviour of Cu-Aβ(4-16) complexes related to Alzheimer’s Disease

The next paper1 in Magda’s series of articles on the redox behaviour of β-amyloids relevant for Alzheimer’s disease has just hit the press.

Here we have been looking at how the presence of a redox-active amino acid, tyrosine (Tyr), affects the oxidation of a Cu(II) attached to the amino terminus of Aβ(4-16).

Although Cu(II) ions, bonded by Aβ(4-42), can be oxidized to highly reactive Cu(III) ions, these complexes do not appear to contribute to the formation of reactive oxygen or nitrogen species (ROS/RNS). So, in this paper we look at the pH-dependent voltammetric response of Aβ(4-16)-Cu(II) complexes to understand the influence of the deprotonation of tyrosine within the complex on the Cu(II)/Cu(III) reaction. The results will help us better understand the scavenging role of tyrosine in quenching highly reactive Cu(III) ions not only in Aβ(4-x)-Cu(II) complexes but also provide clues to the reactive properties of other tyrosine-containing amyloid-metal complexes.

Here we worked together with Steven and Wojtek from our neighbouring Nanoelectrochemistry group to do measuements at high scan rate using microelectrodes. We also used square-wave voltammetry, and especially the frequency (scanr rate) dependence of the reverse current to estimate the rate of the internal electrontransfer between Tyr and Cu(III).

  1. M. Z. Wiloch, S. Linfield, N. Baran, W. Nogala and M. Jönsson-Niedziółka
    Redox behaviour of Cu-Aβ(4-16) complexes related to Alzheimer’s Disease, Electrochim. Acta (accepted), (link)(preprint on ChemRxiv).

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