Pathological ageing involving the accumulation of β-amyloid (Aβ, a cleavage product of Amyloid Precursor Protein (APP)) in Alzheimer’s disease (AD) further illustrates the involvement of mitochondrial dysfunction in neurodegenerative disease: mutant APP and Aβ enter mitochondria and interact with mitochondrial proteins, thereby disrupting the electron transport chain (ETC), increasing reactive oxygen species (ROS) to damaging levels and inhibiting the generation of ATP [2], [3]. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.