Recent data indicate that the protective effects of OLE in the diet of a Tg murine model of Aβ deposition could be traced bask, at least in part, to the increased acetylation of histone 3 and 4, that matched the reduced expression of HDAC-2 [40], whose levels are increased in the AD brain [285,286] and of glutaminyl cyclase (GC), the enzyme responsible for the generation of pE3Aβ, the most aggregating pyroglutamylated derivative of the Aβ1–42 peptide in AD [287]. The gene discussed is HDAC2; the disease is Alzheimer disease.