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According to the amyloid cascade hypothesis, amyloid-β peptides (Aβ) play a causative role in Alzheimer’s disease (AD), of which oligomeric forms are proposed to be the most neurotoxic by provoking oxidative stress. Copper ions seem to play an important role as they are bound to Aβ in amyloid plaques, a hallmark of AD. Moreover, Cu–Aβ complexes are able to catalyze the production of hydrogen peroxide and hydroxyl radicals, and oligomeric Cu–Aβ was reported to be more reactive. The flexibility of the unstructured Aβ peptide leads to the formation of a multitude of different forms of both Cu(I) and Cu(II) complexes. This raised the question of the structure–function relationship. We address this question for the biologically relevant Fenton-type reaction. Computational models for the Cu–Aβ complex in monomeric and dimeric forms were built, and their redox behavior was analyzed together with their reactivity …