Further, the accumulation of an APP-CTF, called C99, a direct precursor of Aβ, in areas vulnerable to AD neurodegeneration neurons [68] results in an altered lipid composition of mitochondrial membranes which interferes with the proper assembly and activity of mitochondrial respiratory supercomplexes, thereby likely contributing to the bioenergetic defects characteristic of AD [69]. The gene discussed is APP; the disease is Alzheimer disease.