Faculty of Medicine, Institute of Physiology, Comenius University in Bratislava, Sasinkova 2, 813 72, Bratislava, Slovakia.
Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Bratislava, Slovakia.
Cell Mol Neurobiol. 2018 Jan;38(1):73-84. doi: 10.1007/s10571-017-0521-1. Epub 2017 Jul 11.
Modern society is characterized by the ubiquity of stressors that affect every individual to different extents. Furthermore, experimental, clinical, and epidemiological data have shown that chronic activation of the stress response may participate in the development of various somatic as well as neuropsychiatric diseases. Surprisingly, the role that stress plays in the etiopathogenesis of Alzheimer's disease (AD) has not yet been studied in detail and is therefore not well understood. However, accumulated data have shown that neuroendocrine and behavioral changes accompanying the stress response affect neuronal homeostasis and compromise several key neuronal processes. Mediators of the neuroendocrine stress response, if elevated repeatedly or chronically, exert direct detrimental effects on the brain by impairing neuronal metabolism, plasticity, and survival. Stress-induced hormonal and behavioral reactions may also participate in the development of hypertension, atherosclerosis, insulin resistance, and other peripheral disturbances that may indirectly induce neuropathological processes participating in the development and progression of AD. Importantly, stress-induced detrimental effects as etiological factors of AD are attractive because they can be reduced by several approaches including behavioral and pharmacological interventions. These interventions may therefore represent an important strategy for prevention or attenuation of the progression of AD.
现代社会的特点是压力源无处不在,这些压力源以不同的程度影响着每个人。此外,实验、临床和流行病学数据表明,慢性应激反应的激活可能参与各种躯体和神经精神疾病的发展。令人惊讶的是,压力在阿尔茨海默病(AD)发病机制中的作用尚未得到详细研究,因此了解得还不够。然而,积累的数据表明,伴随应激反应的神经内分泌和行为变化会影响神经元的内稳态,并损害几个关键的神经元过程。神经内分泌应激反应的介质,如果反复或长期升高,会通过损害神经元代谢、可塑性和存活来直接对大脑产生不利影响。应激引起的激素和行为反应也可能参与高血压、动脉粥样硬化、胰岛素抵抗和其他可能间接诱导参与 AD 发展和进展的神经病理过程的外周紊乱的发生。重要的是,应激诱导的有害作用作为 AD 的病因因素是有吸引力的,因为它们可以通过包括行为和药物干预在内的几种方法来降低。因此,这些干预措施可能代表预防或减缓 AD 进展的重要策略。