Are experimental models useful for analysis of pathogenesis of changes in central nervous system in human diabetes?

Incidence of diabetes and complications associated with the course of the disease make diabetes an important clinical problem. Clinical studies have not provided sufficient data on pathophysiological and therapeutical possibilities of treating the disease and diabetic complications. Published work shows that certain animal models and human diabetes have very similar pathophysiology and clinics. Many similar features have been described in streptozotocin-induced diabetes, which is the most frequently used model. Reported similarities include, e.g., presence of oxidative stress with depletion of endogenous antioxidants, increased lipid peroxidation, changes in metabolism of different cells, development of nephropathy and cataract, decrease of cerebral blood flow, and cognitive function impairment. However, the influence of ageing, long duration of the disease and development of vascular complications (including changes in the walls and endothelium of blood vessels, specific for human diabetes) are difficult to reproduce under laboratory conditions. In the case of central nervous system (CNS), relatively scarce data indicate that observations in animal CNS are different from those in humans. Inter-species differencies among interspecies and the possibility of different pathomechanisms of human diabetes should be taken into consideration when interpreting study results.