Abstract
Long-term stress as well as physiological aging result in similar immunological and hormonal disturbances including hypothalamic-pituitary-adrenal) axis depletion, aberrant immune response (regulatory T-cells, Tregs, and T(h17)-lymphocyte accumulation) and decreased dehydroepian-drosterone synthesis both in the brain and in the adrenal glands. Since the main mechanisms of inflammation control, "prompt" (stress hormones) and "delayed" (Tregs), are broken, serum cytokine levels increase and become sufficient for blood-brain-barrier disruption. As a result peripheral cytokines penetrate into the brain where they begin to perform new functions. Structural and functional alterations of blood-brain-barrier as well as stress- (or age-) induced neuroinflammation promote influx of bone marrow derived dendritic cells and lymphocyte effectors into the brain parenchyma. Thereafter, mass intrusion ofpro-inflammatory mediators and immune cells having a lot of specific targets alters the brain work that we can observe both in humans and in animal experiments. The concept of stressful cognitive dysfunction, which is under consideration in this review, allows picking out several therapeutic targets: 1) reduction of excessive Treg accumulation; 2) supporting hypothalamic-pituitary-adrenal axis and inflammatory reaction attenuation; 3) recovery of dehydroepiandrosterone level; 4) improvement of blood-brain-barrier function.
Highlights
При длительном стрессе и физиологическом старении возникают сходные когнитивные и психологические нарушения
As a result peripheral cytokines penetrate into the brain where they begin to perform new functions
Thereafter, mass intrusion of pro-inflammatory mediators and immune cells having a lot of specific targets alters the brain work that we can observe both in humans and in animal experiments
Summary
Иммунологические нарушения и когнитивный дефицит при стрессе и физиологическом строении. При длительном стрессе и при физиологическом старении возникают сходные иммунологические и гормональные нарушения: гиперактивация и последующее истощение гипоталамо-гипофизарно-надпочечниковой оси, иммунологические нарушения Предложенная нами концепция развития когнитивного дефицита при стрессе и физиологическом старении позволяет определить главные цели терапии: 1) нормализация численности Treg; 2) компенсация истощения гипоталамо-гипофизарно-надпочечниковой оси; 3) компенсация недостаточности дегидроэпиандростерона; 4) восстановление целостности гематоэнцефалического барьера. Long-term stress as well as physiological aging result in similar immunological and hormonal disturbances including hypothalamic-pituitaryadrenal) axis depletion, aberrant immune response (regulatory T-cells, Tregs, and Th17-lymphocyte accumulation) and decreased dehydroepiandrosterone synthesis both in the brain and in the adrenal glands. The concept of stressful cognitive dysfunction, which is under consideration in this review, allows picking out several therapeutic targets: 1) reduction of excessive Treg accumulation; 2) supporting hypothalamic-pituitary-adrenal axis and inflammatory reaction attenuation; 3) recovery of dehydroepiandrosterone level; 4) improvement of blood-brain-barrier function.
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