Altered immune regulation in type 1 diabetes.

Research in genetics and immunology was going on separate strands for a long time. Type 1 diabetes mellitus might not be characterized with a single pathogenetic factor. It develops when a susceptible individual is exposed to potential triggers in a given sequence and timeframe that eventually disarranges the fine-tuned immune mechanisms that keep autoimmunity under control in health. Genomewide association studies have helped to understand the congenital susceptibility, and hand-in-hand with the immunological research novel paths of immune dysregulation were described in central tolerance, apoptotic pathways, or peripheral tolerance mediated by regulatory T-cells. Epigenetic factors are contributing to the immune dysregulation. The interplay between genetic susceptibility and potential triggers is likely to play a role at a very early age and gradually results in the loss of balanced autotolerance and subsequently in the development of the clinical disease. Genetic susceptibility, the impaired elimination of apoptotic ß -cell remnants, altered immune regulatory functions, and environmental factors such as viral infections determine the outcome. Autoreactivity might exist under physiologic conditions and when the integrity of the complex regulatory process is damaged the disease might develop. We summarized the immune regulatory mechanisms that might have a crucial role in disease pathology and development.

[Changes in cognitive function in patients with diabetes mellitus]. / A kognitív funkciók változásai cukorbetegségben.

Patients with diabetes are approximately 1.5 times more likely to experience cognitive decline than individuals without diabetes mellitus. Most of the data suggest that patients with diabetes have reduced performance in numerous domains of cognitive function. In patients with type 1 diabetes, specific and global deficits involving speed of psychomotor efficiency, information processing, mental flexibility, attention, and visual perception seem to be present, while in patients with type 2 diabetes an increase in memory deficits, a reduction in psychomotor speed, and reduced frontal lobe (executive) functions have been found. The complex pathophysiology of changes in the central nervous system in diabetes has not yet been fully elucidated. It is important to consider the patient's age at the onset of diabetes, the glycemic control status, and the presence of diabetic complications. Neurological consequences of diabetes appear parallel to those observed in the aging brain. Neuroimaging studies highlight several structural cerebral changes, cortical and subcortical atrophy, beside increased leukoaraiosis that occurs in association with diabetes. There is supporting evidence from many hypotheses to explain the pathophysiology of cognitive decline associated with diabetes. The main hypotheses pointing to the potential, implied mechanisms involve hyperglycemia, hypoglycemia, microvascular disease, insulin resistance, hyperinsulinism, hyperphosphorylation of tau protein, and amyloid-ß deposition.

[Clinical aspects of the link between diabetes and depression]. / A depresszió és a diabetes kapcsolatának klinikai vonatkozásai.

Diabetes mellitus and depression are public health concerns of the present and, as predicted, also the future. The observation that depression is seen more frequently in diabetic patients compared to the non-diabetic population has been proven by several recent studies. The co-occurrence carries further risks for the affected patients, as depression in diabetics may affect sufficient treatment of diabetes and enhance the development of diabetic complications. These may further worsen depressive symptoms causing a vicious cycle in these patients. In the present paper authors discuss in detail the theoretic and practical issues of the complex two directional relationships between diabetes and depression. Their goal is to draw attention to depression as co-morbidity of diabetes that may interfere with the optimization of diabetic patient's carbohydrate metabolism. If sufficient glycaemic control is not achieved using routine clinical methods depression should be evaluated as a probable cause. If needed, depression should be treated to improve the medical outcomes and quality of life of diabetic patients.