APP and Alzheimer disease: In support of this, it has been shown that cells depleted of endogenous mDNA lacking functional electron transport chains (ETC) are resistant to Aβ toxicity [149]; also, a reduced respiratory capacity and low cytochrome oxidase activity were found in isolated mitochondria exposed to Aβ [150, 151]; transgenic mice expressing mutant APP (amyloid protein precursor) genes exhibit mitochondrial dysfunction, and an AD transgenic mouse line presents early expression of genes encoding mitochondrial proteins and ETC subunits, as an initial cellular change in AD pathology [152].