In vitro experiments further confirmed that Loganin significantly upregulated OPTN expression and downregulated LC3II, p62, PINK1, and Parkin protein expression in Aβ25-35-treated human neuroblastoma cells (SK-N-SH), and significantly ameliorated mitochondrial dysfunction, whereas OPTN silencing counteracted the restoration of mitochondrial function by Loganin, confirming that Loganin may improve cognitive function in AD mice by promoting OPTN-mediated mitophagy (Zhou Y. et al., 2023). The gene discussed is PRKN; the disease is Alzheimer disease.