Specifically, we believe that both CyPD oxidation and CyPD acetylation could play a role in the development of AD, given that: (i) oxidative stress is a hallmark of AD [161,177] and, accordingly, treatment with antioxidants has been shown to be protective from Aβ-mediated insult similarly to genetic inhibition of CyPD [170]; (ii) aging and aging-associated diseases are characterized by a decline in NAD+ levels [178], which can lead to an inhibition of SIRT3 and an increase in CyPD acetylation [121], which induces mPTP opening [121]. The gene discussed is PPID; the disease is Alzheimer disease.