The B vitamin nutritional deficiency applied to the AD transgenic animal model used in our studies was designed to specifically induce one-carbon metabolism alterations resulting in DNA methyltransferase impairment and DNA demethylase improvement, PSEN1 hypomethylation, PSEN1 and BACE1 upregulation and plaque deposition [34,36,37]. The gene discussed is BACE1; the disease is Alzheimer disease.