Alzheimer’s disease (AD) is the most widespread dementia subset, affecting elderly populations worldwide. It has been proved that chronic Type 2 diabetes mellitus (T2DM) is closely related to neurodegeneration, especially AD. T2DM is characterized by the inability of the cell to take up insulin, as well as chronic hyperglycemia. In the central nervous system, insulin has vital regulatory roles, while in chronic hyperglycemia it leads to the formation and accumulation of advanced glycation end products (AGEs). Inflammation plays a crucial role in the development of insulin resistance in AD and T2DM. The microtubule-related protein tau is involved in the pathogenesis of several neurological diseases known as tauopathies and is found to be abnormally hyperphosphorylated in AD and accumulated in neurons. Breakdown of the Blood-Brain Barrier (BBB) found in tauopathies is motivated by chronic neuroinflammation. The development of pro-inflammatory signaling molecules such as cytokines, chemokines and glial cells, neurons and endothelial cells determines the reliability of BBB and immune cell migration into the brain. This review highlights the involvement of several novel pathological molecular mechanisms induced by diabetes that increase AD pathogenesis and the use of anti-diabetic compounds as promising therapeutics for AD.