The reduced efficacy of COX is the most documented change in AD [20, 59-61], which is associated with (1) a deficiency in its structural complex haem-a [62-64]; (2) transmembrane arrest of translocase of the outer mitochondrial membrane 40 kDa (TOMM40) and translocase of inner membrane subunit 23 (TIM23) protein pore related to Aβ and APP processing [65-67]; and (3) mtDNA damage. The gene discussed is APP; the disease is Alzheimer disease.