This review explores the potential of repurposing diabetic drugs to treat Alzheimer's Disease (AD). Type 2 Diabetes Mellitus (T2DM) and AD share several clinical and epidemiological links, including increasing age, insulin resistance, and advanced glycation end products. Insulin resistance in the brain, known as "type 3 diabetes," is hypothesized to play a key role in AD pathogenesis. Preclinical and clinical trials have shown promising results for various antidiabetic drugs, such as metformin, intranasal insulin, incretins, DPP4 inhibitors, PPAR-γ agonists, and SGLT2 inhibitors, in improving cognitive function and reducing AD pathology. Metformin, for instance, has demonstrated positive effects in preclinical trials and some clinical studies, though results vary. Intranasal insulin has shown cognitive benefits in animal models and small human studies, but larger trials have yielded mixed results. Incretins like liraglutide have neuroprotective effects and reduced AD pathology in animal models, with ongoing phase III trials. DPP4 inhibitors have been shown to reduce Aβ load, tau hyperphosphorylation, and neuroinflammation, while PPAR-γ agonists have improved cognitive function and synaptic defects in AD models. SGLT2 inhibitors have neuroprotective effects and reduced Aβ levels in AD models, with some positive findings in human studies. Despite these encouraging results, further research is needed to confirm the therapeutic potential of these drugs in AD.This review explores the potential of repurposing diabetic drugs to treat Alzheimer's Disease (AD). Type 2 Diabetes Mellitus (T2DM) and AD share several clinical and epidemiological links, including increasing age, insulin resistance, and advanced glycation end products. Insulin resistance in the brain, known as "type 3 diabetes," is hypothesized to play a key role in AD pathogenesis. Preclinical and clinical trials have shown promising results for various antidiabetic drugs, such as metformin, intranasal insulin, incretins, DPP4 inhibitors, PPAR-γ agonists, and SGLT2 inhibitors, in improving cognitive function and reducing AD pathology. Metformin, for instance, has demonstrated positive effects in preclinical trials and some clinical studies, though results vary. Intranasal insulin has shown cognitive benefits in animal models and small human studies, but larger trials have yielded mixed results. Incretins like liraglutide have neuroprotective effects and reduced AD pathology in animal models, with ongoing phase III trials. DPP4 inhibitors have been shown to reduce Aβ load, tau hyperphosphorylation, and neuroinflammation, while PPAR-γ agonists have improved cognitive function and synaptic defects in AD models. SGLT2 inhibitors have neuroprotective effects and reduced Aβ levels in AD models, with some positive findings in human studies. Despite these encouraging results, further research is needed to confirm the therapeutic potential of these drugs in AD.