Proceedings of the International scientific and practical conference ―Synergy of Modern Science and Education‖ (June 12-14, 2026) / Publisher website: www.naukainfo.com. – New York, USA, 2026. - 145 p.

119 emotional regulation, and the vulnerability of the nervous system to age-related neurodegenerative changes [5]. The concept of inflammaging is considered one of the key mechanisms underlying age-related diseases. Chronic low-grade systemic inflammation resulting from age-associated changes in immune, metabolic, and neuroendocrine regulation contributes to the development of neurodegenerative, cardiovascular, and metabolic disorders. Age-related dysbiosis may enhance pro-inflammatory processes, impair intestinal barrier function, and promote the progression of inflammaging, whereas a balanced microbiome is associated with reduced systemic inflammation and healthier aging [6]. Chronic systemic inflammation and increased intestinal barrier permeability contribute to the activation of microglia, the principal immune cells of the central nervous system. Prolonged microglial hyperactivation is accompanied by the development of neuroinflammation, neuronal damage, reduced neuroplasticity, and acceleration of age-related cognitive impairment [7]. Age-related remodeling of the endocrine system (neuroendocrine homeostasis) significantly affects cognitive functions [8, 9]. Chronically elevated cortisol levels in older individuals are associated with reduced hippocampal volume, a brain structure that plays a key role in memory, learning, and emotional regulation. Prolonged hyperactivation of the hypothalamic–pituitary–adrenal axis is accompanied by cognitive decline, impaired neuroplasticity, and disturbances in memory formation. Excessive glucocorticoid secretion is considered one of the mechanisms underlying age-related hippocampal neuronal damage. Chronic stress and impaired neuroendocrine regulation may contribute to suppressed neurogenesis, increased neuronal vulnerability to degenerative changes, and accelerated cognitive aging of the brain [10]. Impaired insulin signaling and reduced insulin sensitivity in brain tissues lead to deficient neuronal energy supply and contribute to the development of neurodegenerative processes. Alzheimer’s disease is considered a form of ―type 3 diabetes,‖ characterized by insulin resistance, impaired glucose utilization, oxidative stress, and mitochondrial dysfunction within the central nervous system. These disturbances are accompanied by the accumulation of β-amyloid and hyperphosphorylated tau protein, which are key molecular markers of Alzheimer’s disease. Dysregulation of insulin signaling is also associated with the development of neuroinflammation, reduced neuroplasticity, cognitive decline, and the progression of age-related neurodegenerative changes [11, 12]. A decline in sex hormone and melatonin levels diminishes their neuroprotective effects, thereby accelerating cognitive deterioration. Estrogens play an important role in maintaining the structural and functional integrity of the brain. They are involved in the regulation of neuroplasticity, synaptic transmission, neuronal energy metabolism, and neurogenesis, and also exert antioxidant and neuroprotective effects. Estrogens are particularly important for the functioning of the hippocampus and cerebral cortex, brain regions associated with memory and cognitive functions. Age-related decline in estrogen levels during menopause is associated with impaired cognitive functions, reduced neuroplasticity, and increased neuronal vulnerability to degenerative changes. Estrogen deficiency is considered one of the factors contributing to the development of neurodegenerative processes and the acceleration of cognitive brain aging [13]. Testosterone plays an important role in maintaining cognitive functions, neuroplasticity, and the normal functioning of the central nervous system during aging. Age-related reduction in testosterone levels is associated with deterioration of memory, attention, and executive functions, as well as with an increased risk of cognitive impairment and neurodegenerative processes. Testosterone exerts neuroprotective effects through the regulation of synaptic plasticity, neuronal energy metabolism, antioxidant defense, and reduction of neuroinflammation. Testosterone replacement therapy in elderly men may positively influence certain cognitive functions; however, the effectiveness of this approach depends on age, baseline hormonal status, and the severity of cognitive impairment [14]. Melatonin is considered a multifunctional regulatory molecule involved in the coordination of circadian rhythms, neuroendocrine regulation, immune responses, and cellular metabolic processes. Melatonin has been shown to exert pronounced antioxidant, anti-inflammatory, and neuroprotective effects, contributing to the stabilization of mitochondrial function, reduction of oxidative stress, and protection of neurons against damage. Age-related decline in melatonin production is associated with disturbances in circadian regulation, enhanced neuroinflammation, impaired neuroplasticity, and increased vulnerability of the nervous system to degenerative processes. Melatonin is regarded as one of the important factors supporting cognitive functions and slowing age-related neurodegenerative changes due to its ability to regulate apoptosis, oxidative balance, and cellular energy metabolism [15].