Methionine oxidation in Met-35 of amyloid ß-peptide (Aβ peptide) is thought to be critical for aggregation and neurotoxicity [130] and it was shown that the absence of MsrA modifies Aβ solubility properties and causes mitochondrial dysfunction in a mouse model of Alzheimer’s disease [131,132]. This evidence concerns the gene MSRA and Alzheimer disease.