Oxidative stress is a fundamental element that disrupts mitochondrial function and induces mitochondrial fragmentation during the pathogenesis of AD.34 The mitochondrial hypothesis states that in sporadic, late-onset AD, changes in mitochondrial function affect APP expression and amyloid accumulation in a manner that triggers the pathogenesis of amyloid cascade.35 Correlations have been increasingly recognized between mitochondrial function, Aβ amyloidosis, and tau phosphorylation.36 The gene discussed is APP; the disease is amyloidosis.