Oxidative stress markers as well as high concentrations of copper are found in the vicinity of Aβ amyloid deposits in Alzheimer's disease. The neurotoxicity of Aβ in cell culture has been linked to H₂O₂generation by an unknown mechanism. We now report that Cu(II) markedly potentiates the neurotoxicity exhibited by Aβ in cell culture. The potentiation of toxicity is greatest for Aβ1–42 > Aβ1–40 ≫ mouse/rat Aβ1–40, corresponding to their relative capacities to reduce Cu(II) to Cu(I), form H₂O₂ in cell-free assays and to exhibit amyloid pathology. The copper complex of Aβ1–42 has a highly positive formal reduction potential (≈+500–550 mV versus Ag/AgCl) characteristic of strongly reducing cuproproteins. These findings suggest that certain redox active metal ions may be important in exacerbating and perhaps facilitating Aβ-mediated oxidative damage in Alzheimer's disease.

Significance: We present a method to control the interfacial energy of a liquid metal via electrochemical deposition (or removal) of an oxide layer on its surface. Unlike conventional surfactants, this approach can tune the interfacial tension of a metal significantly (from ∼7× that of water to near zero), rapidly, and reversibly using only modest voltages. These properties can be harnessed to induce previously unidentified electrohydrodynamic phenomena for manipulating liquid metal alloys based on gallium, which may enable shape-reconfigurable metallic components in electronic, electromagnetic, and microfluidic devices without the use of toxic mercury. The results also suggest that oxides—which are ubiquitous on most metals and semiconductors—may be harnessed to lower interfacial energy between dissimilar materials.