It is noteworthy that a recently developed AD rat model engineered to express mutant human APP and PS1 genes was reported to develop cognitive impairment accompanied by AβO production, tau pathology and neuronal loss (Cohen et al., 2013), and a mouse model developed by LaFerla and co-workers expressing Arctic APP at low levels presented enhanced AβO formation and wild-type tau pathology (Chabrier et al., 2012). The gene discussed is ABO; the disease is Alzheimer disease.