[Traumatic brain injury as risk factor of Alzheimer's disease and possibilities of pathogenetic therapy]. / Cherepno-mozgovaya travma kak faktor riska bolezni Al'tsgeimera i vozmozhnosti patogeneticheskoi terapii.

The article examines the potential role of brain mechanical damage as a trigger for the development of neurodegenerative changes. Attention is paid to dysfunction of the neurovascular unit, and disruption of the functional and compensatory capabilities of blood flow. The importance of microhemorrhages that occur in the acute period of injury and the formation of first focal and then diffuse neuroinflammation is emphasized. The importance of mitochondrial dysfunction was separately determined as a significant factor in increasing the risk of developing Alzheimer's disease (AD) in patients after traumatic brain injury (TBI). In TBI, there is a decrease in the expression of tight junction (TC) proteins of endothelial cells, such as occludin, claudin, JP, which leads to increased permeability of the blood-brain barrier. TBI, provoking endothelial dysfunction, contributes to the development of metabolic disorders of ß-amyloid and tau protein, which in turn leads to worsening vascular damage, resulting in a vicious circle that can ultimately lead to the development of AD and dementia. Age-related changes in cerebral arteries, which impair perivascular transport of interstitial fluid, are currently considered as an important part of the «amyloid cascade¼, especially against the background of genetically mediated disorders of glial membranes associated with defective aquaporin-4 (encoded by the APOE4). Studies in animal models of TBI have revealed an increase in tau protein immunoreactivity and its phosphorylation, which correlates with the severity of injury. A comprehensive analysis of research results shows that the cascade of reactions triggered by TBI includes all the main elements of the pathogenesis of AD: disorders of energy metabolism, microcirculation and clearance of cerebral metabolic products. This leads to a disruption in the metabolism of amyloid protein and its accumulation in brain tissue with the subsequent development of tauopathy. Cerebrolysin, by modulating the permeability of the blood-brain barrier, blocks the development of neuroinflammation, reduces the accumulation of pathological forms of proteins and may be slow down the progression of neurodegeneration.

[Treatment of cognitive and non-cognitive symptoms in cerebrovascular disease].

OBJECTIVE: To study the therapeutic efficacy and safety of Ginkgo special extract EGb 761 in the treatment of cognitive and non-cognitive symptoms (anxiety, depression, sleep disorders, activity) in patients with discirculatory encephalopathy (DE) and cognitive impairment. MATERIAL AND METHODS: The study enrolled 45 patients with DE (mean age 60,8±5,9 years). Patients were randomized to treatment with EGb 761 (30 patients) or other drugs (15 patients). Patients underwent neurological examinations, along with cognitive and neuropsychological testing (FAB, MMSE, HADS and other tests). EGb 761 was used in dose 240 mg per day during 24 weeks. RESULTS: By the end of the study, the levels of anxiety and depression decreased (p<0,05) to the 12th and 24th week, respectively. CONCLUSION: The results indicate the efficacy and good tolerability of EGb 761 in the treatment of mental disorders in DE patients with cognitive impairment. The best effect was observed in relation to anxiety.