The preservation of glucose homeostasis is critical for preventing Alzheimer's disease. Hypoglycemia can lead to brain dysfunction, brain damage, and death. A metabolic shift is one of the critical points in midlife aging that increases the risk of late-onset AD. The consumption of brain glucose is reduced in patients with Alzheimer's disease, which suggests an energy deficit . Synaptic inactivity can result from decreased cerebrospinal fluid (CSF) and brain glucose levels, which elevates the likelihood of cognitive impairment and Alzheimer's disease . When the glucose-based antioxidant system stops working as it should in hippocampal slices, it causes big, sudden, and bad changes in how cells work. Metabolic collapse (MC) is the term used to describe this phenomenon . In addition to their glucose-lowering effects, certain antidiabetic pharmaceuticals, including metformin, peroxisome proliferator-activated receptor γ agonists, and glucagon-like peptide-1 receptor agonists, have demonstrated the potential to provide neuroprotective benefits and alleviate ND symptoms .