Proceedings of the International scientific and practical conference ―American Ukrainian Forum of Science and Education‖ (April 13-15, 2026) / Publisher website: www.naukainfo.com. – New York, USA, 2026. - 235 p.

181 Insulin resistance is a condition in which the body does not respond properly to insulin. It can lead to elevated blood glucose levels and weight gain. Individuals may develop prediabetes when blood glucose levels are higher than normal but not high enough to be diagnosed as type 2 diabetes. Insulin acts not only on peripheral organs but is also transported to the brain, where it performs various functions in different regions. The physiological effects of insulin in the brain include modulation of dopamine tone in specific brain areas. Central insulin modulates dopaminergic tonus in the striatum, which may influence regional brain activity and connections [1]. Insulin resistance has a causal relationship with cognitive decline. In particular, elevated insulin resistance markers and proinsulin levels are associated with increased reaction time, indicating reduced cognitive processing speed. Additionally, insulin resistance affects structural changes in the cerebral cortex, particularly reducing the surface area of regions such as the rostral middle frontal cortex. These structural changes mediate approximately 20% of the negative impact of insulin resistance on cognitive function [2]. In elderly individuals, reduced regional cerebral glucose metabolism is observed compared to younger individuals, even after accounting for age-related cortical thinning. Elevated fasting glucose is also associated with reduced brain glucose metabolism in this age group. In young adults, higher insulin resistance is associated with reduced regional cerebral glucose metabolism, whereas this relationship is not observed in older individuals. The strongest effects in young people are seen in the prefrontal, parietal, and temporal cortices, while control conditions involve networks associated with salience, ventral attention, default mode, and somatomotor function. Increased glucose metabolism in neuronal networks is associated with faster reaction time and better psychomotor speed, whereas higher insulin resistance is linked to impaired working memory [3]. Insulin in the central nervous system acts through specific insulin receptors widely distributed in brain regions, particularly the hypothalamus, hippocampus and cortex. Through activation of intracellular signaling pathways, insulin regulates neuronal energy metabolism, glucose utilization, and synaptic plasticity, which is