Frequent cases of pathological brain aging are an important scientific and social problem. Some people have the ability to compensate for the initial manifestations of pathological aging and delay the development of the clinical phenomena of the disease. The concept of “cognitive reserve” allows us to study the possibilities of increasing brain stability in conditions of pathological aging. The identification of the dominant form of thinking, converging or diverging, reveals possible neurophysiological mechanisms of the cognitive reserve. Understanding the mechanisms of formation of individual cognitive styles actualizes the contribution of the “Education” factor to the development of the cognitive reserve. The research material was scientific publications on the topic of work. It was revealed that the “education” factor can realize its protective effect on the pathological aging of the brain due to the formation of an adaptive form of thinking. The data presented in this review make it possible to substantiate the medical and social significance of educational programs for people of mature and older age.

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IntroductionASD is a multifactorial disease. They arise from the interaction of various genetic and environmental factors. These factors affect specific neuronal circuits, oxidative stress, neuroinflammation, mitochondrial dysfunction. This disrupts the development of the nervous system, the formation of synapses, the connection between brain regions, and the size of the brain. Almost 80% of patients with ASD suffer from mitochondrial dysfunction. Therefore, mitochondrial dysfunction plays a crucial role in the pathogenesis of ASD.ObjectivesDeficiency of adenosine-triphosphate (ATP) and abnormal levels of Reactive oxygen species (ROS) cause mitochondrial dysfunction in ASD. This leads to metabolic disorders, disorders of synaptic plasticity and disorders of the immune responseMethodsThe negative association between pathogenic mtDNA mutations and IQ is specific for children with ASD / MD. The overall prevalence of these abnormalities is 1.2 times higher in ASD / MD. ASD, researchers reaffirm that autistic probands carry the burden of mutations in mtDNA, especially mutations that are prone to deleterious effects on OXPHOS. According to a number of researchers, all children with ASD should be screened for MD, given: the high prevalence of abnormal markers of mitochondrial function in ASD compared with the control group; relatively high prevalence of MD in ASD; some children with ASD who have MD may be phenotypically indistinguishable from typical children with ASD; the potential clinical significance of MD in children with ASD.ResultsAccording to a number of researchers, all children with ASD should be screened for MD, given: the high prevalence of abnormal markers of mitochondrial function in ASD compared with the control group; relatively high prevalence of MD in ASD; some children with ASD who have MD may be phenotypically indistinguishable from typical children with ASD; the potential clinical significance of MD in children with ASD.ConclusionsThe pathophysiological mechanisms of ASD are multifactorial. They are largely unclear. But the mitochondrial hypothesis of the pathogenesis of ASD is being clarified. Mitochondrial dysfunction has been identified as a hallmark of diseased neurons in ASD patients, suggesting a critical role for mitochondrial dysfunction in the pathogenesis of ASD and allowing the development of ASD correction by normalizing mitochondrial functions.Disclosure of InterestNone Declared

Relevance:Alzheimer’s disease (AD) is a neurodegenerative pathology that develops mainly in elderly and senile people.Disruption of BDNF transport or suppression of its production appears to be typical for people of old age. Objective: To investigate the influence of Alzheimer’s disease on the secretion of brain factors and correlate with neuropsychological profiles.Material and methods of research:12 men (2) and women (10) with Alzheimer’s disease were examined. The average age of the subjects was 76.25 + 4.89. Methods: MMSE, ADAS-COG, laboratory - BDNF was performed using the G7611 BDNF Emax (R) ImmunoAssaySystem 5 x 96 wells, BDNF Emax® Immunological test.Results:2 patients have mild dementia, 8 patients have moderate dementia, 2 patients have severe dementia. The average age of patients with mild dementia was 72.0 + 1.0. The average MMSE score is 16.7 + 3.4. Correlation analysis showed a close relationship between a pronounced decrease in memory in memory tests (ADAS-COG) and a pronounced decrease in blood BDNF content (r = 0.676). A close statistically significant relationship was found between a low result of the recognition test and a low blood BDNF content (r = 0.598).Conclusion:we assume that blood BDNF is a marker of pathologically accelerated aging of the central nervous system, since low test results for mnestic function are an indicator of severe degeneration in Alzheimer’s disease.

IntroductionCurrently, the number of cases of pathological aging of the CNS, represented by a violation of cognitive functions, is increasing. But there is a social request to prolong the physical and mental activity of older peopleObjectivesThe study of the dynamics of cognitive aging is timely and relevant. The article contains a report on a cohore non-repeating study of higher brain functions at various age periodsMethodsThe average age was 45.1 + 5.7 years. Inclusion criteria: 1. Dextral. Non-inclusion criteria: 1. Clinically significant somatic diseases in their medical history. 2. Mental disorders in their medical history. •Applied neuropsychological, statistical research methods. The research tool was the neuropsychological rapid method including the subtests: •“Memorizing 9 words in three presentations (1st, 2nd, 3rd attempts)”, •“Sequential subtraction”, •“Test of Benton’s visual memory”, •“Solving an arithmetic problem”, •“Overlaid images”, •“Specified flow of associations in 1 minute”, • “Figure of 3 geometric figures”, • “Blind hours”, • “Graph-motor test”, “Delay word reproduction”ResultsThe first cohort 27–40 years old. The second cohort 41–50 years old.Third cohort 51 years old and older. A significant difference in the performance of the graphomotor test between the subjects of the age subgroup of 27-40 years and the subgroup of 41-50 years was statistically confirmed. In older people revealed a much greater number of errors, interruptions of the test than the representatives of the more “young” subgroupConclusionsThe deterioration in the performance of the graphomotor test was the most age-specificDisclosureNo significant relationships.