Биофизика кровообращения при сосудистой деменции и болезни Альцгеймера

Abstract

Modern rational pharmacotherapy allows being provided with a balance of efficacy and safety in clinical geriatrics, which is especially important in patients with neurovascular degeneration, including in the presence of severe forms of vascular comorbidity, requiring multi–component therapy, under the condition of active multidisciplinary and interdepartmental impact. Dementia in its origin is mixed and it is extremely difficult to divide into parts its primary degenerative or vascular component. The differentiated approach is determined by the heterogeneity of the pathological process, which common is the relationship of cerebral vascular damages with the development of the brain symptoms damage. The problem of nosological independence of Alzheimer’s disease is the subject of discussion for patients of older age groups (especially in people 65 years and older). The genesis of mnestic–intellectual disorders is due not so much to primary–degenerative as vascular changes, especially at the level of the microcirculatory canal. The modern problem of neurodegeneration has a neurophysiological, biophysical, gerontological, geriatric and strategic practical orientation since the diagnosis of the cause of the disease determines the choice of adequate treatment. Due to a large number of pathogenetical mechanisms, there is no single and standardized method of treatment for vascular dementia and Alzheimer’s disease. In any case, prevention of the development and progression of vascular dementia and Alzheimer’s disease should take into account the etiological mechanisms of its occurrence, because it will vary in patients with failures of small vessels, occlusive damages of the main arteries of the head or an embolism of cardiogenic origin. In patients with failures of small vessels, the main direction of therapy should be the normalization of blood pressure, which leads to improved cognitive functions. At the same time, excessive lowering of blood pressure can provoke an increase in mnestic-intellectual disorders, possibly caused by a secondary decrease in cerebral blood flow due to a violation of autoregulation. Biophysics of blood circulation in Alzheimer’s disease is characterized by disorders of laminar blood flow and cerebral hypoperfusion. As a result, failure intracellular metabolism, there is a cascade of changes in neurons associated with the processes of excitotoxicity and oxidant stress, which in turn stimulates amyloidogenesis. Experimental and 25-year observations have shown that the long–existing state of hypoperfusion leads to hippocampal disorders. This process is accompanied by memory impairment, structural changes in the capillaries in the hippocampus, impaired glucose and protein metabolism, β–amyloid deposition, activation of glial tissue, the death of hippocampal neurons.