A paramount strategy in this study was to explore theeffect ofTP* on Cu2+ coordination to PrP, another AD-related copper-bindingprotein, beyond Aβ(1–X) species.85 PrPC is one of the main copper-binding proteins at thesynapse and it has been recently implicated with AD-neurotoxic mechanisms;it colocalizes in the amyloid plaques of AD patients86−89 and binds Aβ monomers and oligomers,90,91 triggering neurotoxic pathways and promoting Aβ uptake.92 This is indeed the first time that the impactof a copper chelator with therapeutic potential for AD in copper bindingto PrPC is evaluated. This evidence concerns the gene PRNP and Alzheimer disease.