APP and Alzheimer disease: The accumulation of Aβ peptides or of the precursor APP inside the mitochondria (Anandatheerthavarada et al., 2003; Hansson Petersen et al., 2008) and even the interaction of Aβ peptides with some component of the mitochondrial matrix (Lustbader et al., 2004) would be the most straightforward and rational explanations to justify the mitochondrial dysfunctions in the animal models of AD.