Considering the multiple hypotheses regarding the pathogenesis of AD (i.e., inflammation, oxidative stress, mitochondrial dysfunction, altered metal homeostasis, axonal transport deficits, the extracellular accumulation of Aβ peptides, and the intracellular accumulation of hyperphosphorylated tau proteins), there is an urgent need to improve treatment [12,18]. The gene discussed is MAPT; the disease is Alzheimer disease.