Indeed, many of the principal hallmarks of aging (e.g., oxidative stress, mitochondrial dysfunction, accumulation of oxidatively damaged molecules, impaired autophagy, disruption of Ca2+ homeostasis, aberrant neuronal network excitability, and neuroinflammation) have also been documented in AD, and these changes may promote amyloidogenic APP processing and Tau pathology and vice versa [161, 162]. This evidence concerns the gene APP and Alzheimer disease.