The negative influence of diabetes mellitus (DM), both insulin-dependent and non-insulin dependent on the level of cognitive functions has been proven in multiple studies. DM is considered one of the primary risk factors for vascular dementia. The results of epidemiological studies suggest that DM increases the risk of Alzheimer's disease (AD) by 50-100% as well. The effect is largely independent of other, so-called vascular risk factors. The association could be explained by chronic brain hypoperfusion, the toxic effects of hyperglycaemia itself (damage to the blood-brain barrier), and the mediating role of insulin. Since the discovery of insulin and its receptors in the central nervous system, brain has no longer been considered an insulin-independent organ. Physiologic concentrations of insulin exert a beneficial effect on cognition. Too low a concentration of insulin in the periphery as well as hyperinsulinaemia, usually as a result of insulin resistance, both can significantly increase the risk of AD (even in people not suffering from DM!). There are several mechanisms through which central hypoinsulinaemia can accelarate the generation of Alzheimer pathology: decline of glucose utilization, particularly in the hippocampus and enthorinal cortex; increased oxidative stress associated with the synthesis of advanced glycation endproducts (AGE); increased tau protein phosphorylation and neurofibrillary tangle formation; increased aggregation of beta-amyloid protein secondary to the insulin-degrading enzyme (IDE) inhibition. Therapeutic strategies targeted at restoring the balance in insulin metabolism in AD – applying nasal insulin or using thiazolidinedions – are currently in the phase of clinical trials.