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However, all these treatments are symptomatic and cannot prevent or reverse AD pathology ( Figure 1 ) ( Figure 1 Biological characteristics of GLP-1 In the 1980s, a new glucagon-like peptide, produced from proglucagon cleavage, was discovered to stimulate insulin secretion ( GLP-1, a 36-amino acid peptide, is produced in enteroendocrine L-cells of the distal small bowel and colon ( The effect of GLP-1 depends on blood glucose levels since it can only potentiate glucose-stimulated insulin secretion from islet beta cells in the hyperglycemic state rather than in the normal blood glucose state ( Tissue distribution of GLP-1R GLP-1 mediates its effects by binding to its receptor, the GLP-1R, which is a sevenfold transmembrane G-coupled receptor that increases levels of cAMP by activating adenylate cyclase ( In the peripheral system, GLP-1R mediates the actions of GLP-1 via the incretin axis, in which stimulation of the GLP-1R with GLP-1 primarily triggers insulin release from islet cells in a glucose-dependent manner and inhibits glucagon secretion from islet cells ( s coupling pathway (114)

(Exenatide is FDA approved as monotherapy for the management of T2DM.) Explicitly stated in the guideline for patients requiring dual or triple therapy, the AACE/ACE preferentially recommends the addition of a GLP-1 receptor agonist or a DPP-4 inhibitor (sitagliptin, saxagliptin), citing their efficacy and safety profiles as preferred agents over TZDs or sulfonylureas (SUs)

In contrast, high glucose levels primarily trigger insulin secretion, which is amplified by GLP-1 receptor stimulation in GLP-1R-MIN-6 cells

As more research emerges, GLP-1 medications may become a powerful adjunct therapy in rheumatologysupporting traditional treatments and improving long-term outcomes