Simultaneously there is increased expression of BACE1 as well as elements of the γ-secretase complex (Blasko et al., 2004; Chen et al., 2004; Nadler et al., 2008; Loane et al., 2009; Zohar et al., 2011) – all of which would predict that there would be increased processing of APP toward Aβ leading to great interest in the possibility that similar neurotoxic mechanisms might be operative in both AD and TBI. The gene discussed is APP; the disease is Alzheimer disease.