Alzheimer disease (AD) is the most common form of dementia. Different pathogenic processes have been studied that underlie characteristic changes of AD, including A beta protein aggregation, tau phosphorylation, neurovascular dysfunction, and inflammatory processes. Insulin exerts pleiotropic effects in neurons, such as the regulation of neural proliferation, apoptosis, and synaptic transmission. In this setting, any disturbance in the metabolism of insulin in the central nervous system (CNS) may put unfavorable effects on CNS function. It seems that disturbances in insulin metabolism, especially insulin resistance, play a role in most pathogenic processes that promote the development of AD. In this article, the relationships of disturbances in the metabolism of insulin in CNS with A beta peptides aggregation, tau protein phosphorylation, inflammatory markers, neuron apoptosis, neurovascular dysfunction, and neurotransmitter modulation are discussed, and future research directions are provided.