Diabetes and memory: new data
Why does memory deteriorate in diabetes mellitus?
S.Kholin, Scientific.ruOver the past 30 years, the incidence of diabetes has increased significantly.
According to Polonsky (The Past 200 Years in Diabetes, N Engl J Med 2012), almost 27% of the population over 65 years of age suffers from this endocrine disease. In addition to the symptoms that are quite unpleasant for the patient, diabetes mellitus is dangerous for the development of a whole group of serious complications, many of which can lead to disability and death. First of all, it concerns vascular disorders. The fact is that as the concentration of glucose in the blood increases, deep irreversible changes form in the capillary wall of all body tissues. This phenomenon is called diabetic angiopathy, characterized by a violation of vascular permeability, an increase in their fragility, the development of atherosclerosis, a tendency to thrombosis, etc. Because of this, the supply of oxygen and nutrients to tissues significantly worsens. In other words, chronic, gradually progressive hypoxia (oxygen starvation) of organs and tissues develops. It leads to complications such as loss of vision, disruption of the heart and kidneys, gangrene of the extremities, deep metabolic disorders (accumulation of acetone in the blood, acidosis, violation of water-electrolyte metabolism, inhibition of protein synthesis, acceleration of fat breakdown, etc.).
In addition to the above deviations in diabetes mellitus, the functioning of the central nervous system gradually worsens. This is manifested by various symptoms, including fatigue, decreased memory and impaired learning ability. Often patients have problems with intelligence. For example, a link has recently been proven between diabetes mellitus and the appearance of both vascular dementia (Crane et al., Glucose Levels and Risk of Dementia, N Engl J Med 2013) and Alzheimer's disease (Moeller et al., Nephrogenic Diabetes Insipidus: Essential Insights into the Molecular Background and Potential Therapies for Treatment, Endocrine Reviews, 2013). In addition, diabetic patients are almost 3 times more likely to have a stroke compared to people with normal glucose metabolism. However, many links and features of the appearance of such pathological changes in brain tissue have not been studied in detail to date.
A group of scientists from the USA led by Deepti Navaratna (Navaratna et al., Cerebrovascular degradation of TRKB by MMP9 in the diabetic brain, J. Clin. Invest., 2013) a complex study was conducted, the purpose of which was to identify the mechanisms of formation of cerebrovascular dysfunctions in violation of glucose metabolism. To do this, experimental diabetes was simulated in laboratory animals using streptozotocin, a substance that selectively affects beta cells of the pancreas (they produce insulin). This model is the most complete, since the main cause of diabetes is known to be insulin deficiency.
As a result of the experiment, it was found that in diabetes, the activity of an enzyme called matrix metalloproteinase-9 (MMP9) significantly increases. This is due to the accumulation of glycated (glycosylated) endoproducts in the blood, that is, complexes of organic substances (mainly proteins) with carbohydrates. Metalloproteinase, in turn, begins to destroy a very important receptor TRKB (neurotrophic tyrosine kinase receptor), responsible for the production of brain trophic factor (BDNF) by microvessels. The latter is designed to ensure the normal functioning of brain neurons and their interaction with each other; in other words, it performs the role of a specific and effective neuroprotector. Therefore, when BDNF deficiency occurs as diabetes mellitus progresses, there is a stable deterioration of the neurons of the central nervous system, called cerebrovascular degeneration. The brain becomes defenseless from the effects of tissue hypoxia and other adverse factors that necessarily accompany chronic insulin deficiency in the body. Due to this pattern of events, the structural and functional parameters of brain neurons deteriorate significantly, and, as a result, memory and learning ability decrease.
Thus, it is proved that the deterioration of brain activity in diabetes mellitus is provoked by an increase in the activity of the enzyme metalloproteinase-9. The development of pharmaceutical agents that inhibit the work of this enzyme is a new promising way to protect the cells of the central nervous system in diabetes mellitus.
Portal "Eternal youth" http://vechnayamolodost.ru30.08.2013