It is the first rodent model to display a full pathology consistent with human AD through an acceleration of age-dependent accrual of the β-amyloid protein (Aβ) in the presence of wild-type tau and all within the animal’s normal lifespan: dense and diffuse amyloid plaques, high levels of soluble Aβ oligomers, cerebral amyloid angiopathy, hyperphosphorylated tau and paired helical filaments, cerebral vacuoles (Hirano bodies, granulovacuolar), robust neuroinflammation, cognitive impairment, and substantial cortical neuronal loss [3]. The gene discussed is MAPT; the disease is Cognitive impairment.