A current National Institute of Health (NIH) ontology of candidate targets in AD includes amyloid-related mechanisms, tau pathways, apolipoprotein E e-4 (ApoE-4), lipid metabolism, neuroinflammation, autophagy/proteasome/unfolded protein response, hormones/growth factors, dysregulation of calcium homeostasis, heavy metals, mitochondrial cascade/mitochondrial uncoupling/antioxidants, disease risk genes and related pathways, epigenetics, and glucose metabolism [37, 38]. This evidence concerns the gene APOE and Alzheimer disease.