Vitamins B deficiency, and the resulting hyper-homocysteinemia, may affect cognition with loss of total brain volume and cognitive and memory decline [46],[47], through pathways involving redox potentials with altered calcium influx, tau protein and beta-amyloid accumulation, which are associated with AD pathogenesis [48]–[50], apoptosis and neuronal death [51]. The gene discussed is MAPT; the disease is hyperhomocysteinemia.