Also changes in histone tail modifications have been observed in post-mortem AD brains, including decreased levels of H3 acetylation in the temporal lobe (Zhang et al., 2012), and increased levels of the histone deacetylases HDAC6 and HDAC2, the first leading to increased tau phosphorylation and the latter repressing genes required for learning and memory (Ding et al., 2008; Gräff et al., 2012). This evidence concerns the gene HDAC2 and Alzheimer disease.