CKB and early-onset autosomal dominant Alzheimer disease: This synergism between two common forms of protein damage suggests a potential role for isoAsp formation in oxidation of CKB in vivo. We note here that the histidines adjacent to Asn-28 and Asp-190 are susceptible to oxidative modification by 4-hydroxy-2-nonenal, a byproduct of peroxidation that is increased in Alzheimer's disease [61].