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However, whether mitochondrial quality control (MQC) can be targeted for therapeutic interventions remains uncertain. This study uses clinical samples, molecular biology techniques, pharmacological interventions, and genetic approaches to investigate the significance of NAD+ levels in cross\u2010species models of PD. These results reveal that treatment of rotenone\u2010incubated cells with NAD+ boosters (such as NMN, siCD38, and NAT) increases UPR\n                    <jats:sup>mt<\/jats:sup>\n                    \/mitophagy\u2010related MQC, reduces pro\u2010inflammatory cytokine expression, inhibits apoptosis, and strengthen redox reactions. In vivo, NMN supplementation inhibits motor deficit and forestalls the neuropathological phenotypes of MPTP\u2010induced PD mice, which are required for the\n                    <jats:italic>atf4<\/jats:italic>\n                    \u2010related mitochondrial UPR pathway. 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