Mutation of the Phe20 residue in Alzheimer's amyloid beta-peptide might decrease its toxicity due to disruption of the Met35-cupric site electron transfer pathway.

Abstract excerpt

It has been proposed that the Met residue in the C-terminal domain of the Alzheimer's disease beta-amyloid peptide (betaA) serves as a source of electrons for the Cu(II)-catalyzed reduction of molecular oxygen to hydrogen peroxide. Mechanistically, this process would require the long distance electron transfer from the thioether sulfur to the peptide-bound copper. Therefore, the electron transfer pathways between...

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