Although there is an abundance of evidence indicating the presence of oxidative stress and mitochondrial dysfunction in both AD and PDD, evidence concerning the DLB brain is much more limited; however, there have been reports of oxidative damage in the DLB brain even at early stages of the disease—in particular, involving increases in the levels of advanced glycation end products (AGEs) and their receptors as well as in the lipoxidation of α-synuclein in the fCX (Dalfo and Ferrer, 2008), even prior to alterations in α-synuclein aggregation. This evidence concerns the gene SNCA and Alzheimer disease.