[Alzheimer's disease and diabetes - the common pathogenesis].

Epidemiological studies presented evidence that Alzheimer's disease and type 2 diabetes share common features in their pathophysiology and clinical patterns. Insulin resistance is a characteristic feature of both diseases. According to the pathomechanism, inflammatory, metabolic, and an atypical form based on the deficiency of zinc ions can be distinguished. Glucose metabolic disorders, related to Alzheimer's disease, are type 2 diabetes, and prediabetes/metabolic syndrome. Based on the common pathophysiological patterns of these two diseases, Alzheimer's disease is customary called type 3 diabetes. In the research on dementias, insulin resistance stands in the highlight for its documented harmful effects on cognitive function and causes dementia. Insulin-like growth factor also influences cognitive functions. Reduced input of this hormone into the brain may also cause dementia, however literary data are controversial. In Alzheimer's disease, deposition of amyloid ß in the brain, hyperphosphorylation of tau proteins and dysruption of neurofibrilles are characteristic. Amyloid ß is co-secreted in the ß-cells of the pancreas with insulin. Amyloid ß and hyperphosphorylated tau protein were detected in the Langerhans islets by autopsy. Amyloid deposits, found in the pancreas and brain presented similarities. As a consequence of hyperglycemia, glycation endproducts cause the development of amyloid plaques, dysruption of neurofibrilles, and activated microglia, all are typical to Alzheimer's disease. Continuous hyperglycemia leads to oxidative stress, which used to play significant role in the development of both diseases. Low-grade inflammation is also a significant pathophysiological factor in both disorders. The sources of inflammation are proinflammatorical adipocytokines, dysbacteriosis, metabolic endotoxaemia, caused by lipopolysaccharides, and high fat diet which also lead to insulin resistance. Based on recent data, microbial amyloid, the main product of bacteria, is also contributing to the pathophysiology of the human central nervous system. Alzheimer's disease is a heterogeneous disorder, and as yet there is no effective therapy. Encouraging results have emerged by using intranasal insulin spray. Insulin sensitizers like metformin, thiazolidines have also resulted in improvements in cognitive functions, mainly in animal experiments. Glucagon-like peptide-1, beyond its insulin-stimulating effect, also has central pleiotropic influences. Research results with the application of these molecules seem to be enouraging. More recently, glucagon-like peptide-1, and glucose-dependent insulinotropic peptide were administered together, with promising early results. The real breakthrough has not yet arrived. For the time being we have to endeavour to the prevention of both chronic diseases via a more healthy life-style.