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The key pathological hallmarks of AD include amyloid-beta (A) plaque accumulation, neurofibrillary tangles of hyperphosphorylated tau, chronic neuroinflammation, oxidative stress, and mitochondrial dysfunction (Lv et al., 2020)

It has multiple actions including: potentiation of glucose-mediated insulin secretion mechanisms identified: increased -cell proliferation, resulting in an increase -cell mass (Fusco et al, 2017) stimulation of insulin biosynthesis at the translational level, helping to maintain -cell insulin stores and secretory capacity (Baggio & Drucker, 2007) because the GLP-1 effect is glucose-dependent (there is more insulin release when glucose levels are elevated, but less effect when glucose levels are normal), GLP-1 agonists have a lower risk for producing hypoglycemia compared to sulfonylureas (that chronically stimulate insulin release, independent of glucose concentration) suppression of postprandial glucagon release Evidence indicates that stimulation of pancreatic cells by GLP-1 increases their glucose sensitivity, resulting in less glucagon release at any glucose level (Baggio & Drucker, 2007)

In preclinical models, simultaneous deficiency in NAD+ and GSH is associated with accelerated mitochondrial dysfunction