APP and Alzheimer disease: In postmortem evaluations, it was evidenced that nonglycosylated full-length and C-terminal truncated APP had been accumulated exclusively in the protein import channel of mitochondria of AD brains (specially higher accumulation in AD-vulnerable regions, such as cortex, hippocampus, and amygdala), by forming stable complexes with the outer membrane translocase and/or the inner membrane translocase; the effect of such association could inhibit the entry of nuclear encoded Cyt C oxidase protein, thus diminishing its activity in mitochondria and increasing the levels of H2O2.