In AD, global DNA hypomethylation in postmortem tissue, also confirmed by monozygotic twin studies, but also differential methylation of specific genes like ANK1, MCF2L, STK32C, LRRC8B, MAP2, and S100B, all associated with neuronal function, as well as methylation changes at key AD risk genes such as APP and ADAM17 have been reported, but also other epigenetic changes and also changes in factors upstream of TAU pathology (e.g. CDK5, GSK-3 beta) [2]. This evidence concerns the gene S100B and Alzheimer disease.