Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are both chronic, progressive disorders linked to aging, with increasing evidence of their clinical and epidemiological connections. Both conditions are associated with insulin resistance, advanced glycosylation end products, obesity, and insulin resistance. Insulin resistance in the brain is thought to play a key role in AD pathogenesis, earning it the name "type 3 diabetes." This review explores the potential of repurposed diabetic drugs, such as metformin, insulin, incretins, DPP4 inhibitors, PPAR-γ agonists, and SGLT2 inhibitors, in treating AD. Preclinical and clinical studies suggest that these drugs may improve cognitive function and reduce AD pathology. Metformin has shown benefits in preclinical trials, including improved memory and reduced amyloid burden. Clinical trials have yielded mixed results, with some showing reduced cognitive decline and others indicating increased AD risk. Insulin, particularly intranasal insulin, has shown promise in improving cognitive function and reducing amyloid plaque. Incretins like GLP-1 agonists have demonstrated neuroprotective effects and reduced amyloid burden. DPP4 inhibitors have shown benefits in reducing amyloid and tau pathology. PPAR-γ agonists have shown potential in improving cognition and reducing neuroinflammation. SGLT2 inhibitors have shown neuroprotective effects and improved cognitive function. Despite promising results, challenges remain, including drug delivery, side effects, and the need for further clinical trials. The overlap between T2DM and AD suggests that anti-diabetic drugs may offer a synergistic approach to AD treatment.Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM) are both chronic, progressive disorders linked to aging, with increasing evidence of their clinical and epidemiological connections. Both conditions are associated with insulin resistance, advanced glycosylation end products, obesity, and insulin resistance. Insulin resistance in the brain is thought to play a key role in AD pathogenesis, earning it the name "type 3 diabetes." This review explores the potential of repurposed diabetic drugs, such as metformin, insulin, incretins, DPP4 inhibitors, PPAR-γ agonists, and SGLT2 inhibitors, in treating AD. Preclinical and clinical studies suggest that these drugs may improve cognitive function and reduce AD pathology. Metformin has shown benefits in preclinical trials, including improved memory and reduced amyloid burden. Clinical trials have yielded mixed results, with some showing reduced cognitive decline and others indicating increased AD risk. Insulin, particularly intranasal insulin, has shown promise in improving cognitive function and reducing amyloid plaque. Incretins like GLP-1 agonists have demonstrated neuroprotective effects and reduced amyloid burden. DPP4 inhibitors have shown benefits in reducing amyloid and tau pathology. PPAR-γ agonists have shown potential in improving cognition and reducing neuroinflammation. SGLT2 inhibitors have shown neuroprotective effects and improved cognitive function. Despite promising results, challenges remain, including drug delivery, side effects, and the need for further clinical trials. The overlap between T2DM and AD suggests that anti-diabetic drugs may offer a synergistic approach to AD treatment.