Here, we extend that analysis in vivo and observe that, compared to 5xFAD mice without NMN treatment, several UPRmt chaperone proteins (ATF4, ATF5, and CHOP), UPRmt protease proteins (YME1L1, CLpP, and LONP1), and mitophagy targets (PINK1, Parkin, FUNDC1, OPTN, and Becline 1) were upregulated in the hippocampus after NMN supplementation (Fig. 5a–d), similar to what has previously been shown in AD cell models, presumably to maintain protein homeostasis within mitochondria in mice brain. The gene discussed is OPTN; the disease is Alzheimer disease.