AD patients are characterized by a progressive cognitive decline and behavioral changes due to the dysregulation of two prion-like proteins: (i) Aβ, resulting from the abnormally processed amyloid precursor protein (APP) though greater activity of β-secretase-1 (BACE1), and (ii) tau, a microtubule-associated protein that promotes the polymerization and stabilization of microtubules (MT) under the regulatory control of several kinases and phosphatases [171,172]. The gene discussed is BACE1; the disease is Alzheimer disease.