SAMe depletion in AD animal models and in vitro has been shown to perturb DNA methylation with resultant increases in the expression of Amyloid Beta Precursor Protein (APP), Presenilin-1 (PS1) and Beta-Secretase 1 (BACE1) genes, stimulating Aβ production and neurodegeneration (13–16). The gene discussed is BACE1; the disease is Alzheimer disease.