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.

182 essential for learning and memory. In insulin resistance, insulin signaling is disrupted at receptor and post-receptor levels, leading to reduced neuronal glucose uptake, impaired cellular energy supply, and dysregulated neuronal activity. This results in decreased synaptic efficiency and plasticity, particularly in structures responsible for cognitive functions. Additionally, brain insulin resistance is associated with impaired lipid metabolism regulation, increased oxidative stress, and neuroinflammation, further exacerbating neuronal dysfunction [4]. Insulin resistance is considered one of the key mechanisms in the development of Alzheimer’s disease, as it disrupts insulin signaling in the central nervous system. This reduces the neuroprotective effects of insulin, which normally support energy metabolism, neuronal survival and synaptic plasticity. In insulin-resistant states, brain glucose utilization decreases leading to neuronal energy deficiency and impaired function. This promotes pathological processes such as increased β-amyloid production and tau protein hyperphosphorylation, which are hallmarks of Alzheimer’s disease. Additionally, impaired insulin signaling enhances neuroinflammation and oxidative stress, further contributing to neurodegeneration and cognitive decline [5]. The insulin receptors in the brain are unevenly distributed with the highest density in the hippocampus and cerebral cortex—regions responsible for cognition, learning and memory. Upon insulin binding, an intracellular signaling cascade is activated, including receptor autophosphorylation and insulin receptor substrate (IRS) activation. This triggers major signaling pathways such as PI3K/Akt and MAPK. These pathways are crucial for regulating neuronal growth, survival and synaptic plasticity, which are essential for cognitive processes. They also regulate neuroinflammation, as their dysregulation in glial cells promotes inflammatory mediator production. Insulin also exerts neuroprotective effects by reducing β- amyloid accumulation and preventing its synaptic binding. Through PI3K/Akt signaling, insulin inhibits glycogen synthase kinase-3β (GSK-3β), which is involved in tau phosphorylation—a key pathological marker of Alzheimer’s disease [6]. So, insulin resistance is an important metabolic disorder that affects not only peripheral organs but also brain function. It leads to reduced neuronal glucose