Alzheimer’s Beta-amyloid peptide as a source of neurotoxic free radicals: the role of structural effects

This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid Beta-peptide (Beta AP), involved in the pathogenesis of Alzheimer’s disease. The CuII-catalysed oxidation of C-terminal Met35 in Beta AP depends on the secondary structure of the peptide. That seems to be the key to the known propensities of this peptide to form reactive oxygen species and free radicals. The pro-oxidant character of Beta AP is not associated with its Beta-sheet insoluble form. On the contrary, the alfa-helically organised structure is responsible for Beta AP redox-related cytotoxicity.