Alzheimer’s Disease (AD) and Type 2 Diabetes Mellitus (T2DM) are major public health concerns with growing socioeconomic impacts due to increasing life expectancy. AD is marked by the accumulation of amyloid-beta (Aβ) plaques and hyperphosphorylated tau protein tangles in the brain, leading to synaptic dysfunction, neuronal loss, and cognitive decline. T2DM is characterized by insulin secretion defects and insulin resistance, resulting in elevated blood glucose levels and associated vascular complications such as cardiovascular disease, stroke, neuropathy, retinopathy, and nephropathy. In this chapter it has been explaned the strong link between AD and T2DM, despite their apparent differences. Both diseases share risk factors like aging, obesity, apolipoprotein E4 presence, elevated cholesterol, oxidative stress, mitochondrial dysfunction, inflammation, and insulin resistance. Insulin resistance, a hallmark of T2DM, is increasingly seen as a critical factor in AD development, leading to the concept of “type 3 diabetes.” The relationship between diabetes and cognitive function is crucial as cognitive deficits can impair diabetes management and independence. Diabetes-specific risk factors and comorbidities, especially the duration of diabetes, are linked to cognitive dysfunction. Chronic hyperglycemia significantly increases dementia risk, with elevated postprandial glucose levels correlating with more severe cognitive impairment. T2DM patients often have higher plasma levels of Aβ peptides, which are involved in AD pathology. Insulin dysregulation in diabetes may affect Aβ production and clearance, raising extracellular Aβ levels.