Thus, growing evidence supports intraneuronal accumulation of Aβ as an early event in the course of the pathology, and there are studies in at least seven other murine AD models (including 5xFAD, amyloid precursor protein (APP)/tau, APP751SL/PS1 KI, APPE693Δ and TBA2) (Iulita et al., 2014; Tomiyama et al., 2010; Wirths & Bayer, 2010) that also show the presence of intraneuronal Aβ prior to extracellular accumulation, independent of the mutation they carry. The gene discussed is APP; the disease is Alzheimer disease.