Institute of Biosciences and Applications, NCSR Demokritos, Athens, Greece.
Life and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Adv Exp Med Biol. 2023;1423:303-315. doi: 10.1007/978-3-031-31978-5_31.
Chronic stress and high levels of the main stress hormones, and glucocorticoids (GC), are implicated in susceptibility to brain pathologies such as depression and Alzheimer's disease (AD), as they promote neural plasticity damage and glial reactivity, which can lead to dendritic/synaptic loss, reduced neurogenesis, mood deficits, and impaired cognition. Moreover, depression is implicated in the development of AD with chronic stress being a potential link between both disorders via common neurobiological underpinnings. Hereby, we summarize and discuss the clinical and preclinical evidence related to the detrimental effect of chronic stress as a precipitator of AD through the activation of pathological mechanisms leading to the accumulation of amyloid β (Aβ) and Tau protein. Given that the modern lifestyle increasingly exposes individuals to high stress loads, it is clear that understanding the mechanistic link(s) between chronic stress, depression, and AD pathogenesis may facilitate the treatment of AD and other stress-related disorders.
慢性应激和主要应激激素（GC）水平升高与易患抑郁症和阿尔茨海默病（AD）等脑部疾病有关，因为它们会促进神经可塑性损伤和神经胶质反应，从而导致树突/突触丢失、神经发生减少、情绪缺陷和认知障碍。此外，抑郁症与 AD 的发展有关，慢性应激是通过共同的神经生物学基础将这两种疾病联系起来的潜在因素。因此，我们总结和讨论了与慢性应激作为导致淀粉样蛋白β（Aβ）和 Tau 蛋白积累的病理机制激活从而导致 AD 的促发因素相关的临床前和临床证据。鉴于现代生活方式使个体越来越多地面临高压力负荷，显然，了解慢性应激、抑郁症和 AD 发病机制之间的机制联系可能有助于 AD 和其他与应激相关的疾病的治疗。
