Взаємозв’язок психофізіологічних показників та імунного статусу в процесі старіння

Abstract

Abstract. Biological aging of the human body is a natural, gradual decline in the functions of cells, tissues, and organs, accompanied by a reduced capacity to adapt to stress and recover. The immune system progressively and inexorably loses its protective control; instead, it contributes to cellular damage within organs – not only through chronic systemic inflammation and oxidative stress, but also via impairments in phagocytic activity and in both the humoral and cellular components of the immune response. Humoral immunity defends the body using specialized proteins (antibodies, or immunoglobulins) that circulate in bodily fluids (such as blood, lymph, and interstitial fluid). As control over infectious agents diminishes, the human body becomes increasingly vulnerable to bacterial and viral pathogens. In T- and Blymphocytes, which are responsible for cellular immunity, receptor-ligand interactions are disrupted, thereby affecting immune response regulation and the body's defense against infectious pathogens. Furthermore, these same processes impact neurogenesis, leading to neuroinflammation and the impairment of synaptic and intercellular communication within the brain. These disturbances alter not only the connections between cells but also the DNA within the cells themselves. Since telomeres serve to prevent the degradation of genetic material, these pathological changes result in the shortening of these protective segments located at the ends of chromosomes. Chronic stress and reduced synthesis and release of neurotransmitters –occurring alongside accelerated telomere shortening in DNA – exacerbate immunosenescence. Furthermore, during cellular aging, senescent cells produce proinflammatory cytokines, chemokines, and matrix metalloproteinases; these damage the cellular structures of organs and tissues, thereby sustaining a persistent pro-inflammatory state within the body