Research has shown that the abnormal accumulation of advanced glycation end-products (AGEs) due to hyperglycemia increases the production of reactive oxygen species (ROS), which in turn activates downstream APP-related pathways, enhances Aβ production, and upregulates NAD + -dependent deacetylase sirtuin 1 (Sirt1) and glucose-regulated protein 78 (GRP78), leading to neuronal cell death pathways and ultimately contributing to the onset of cognitive impairments (Kong et al., 2020). This evidence concerns the gene SIRT1 and Hyperglycemia.