Department of Biochemistry and Genetics, La Trobe Institute for Molecular Science, La Trobe University, Bundoora, Victoria, 3083, Australia.
School of Biomedical Sciences, The University of Queensland, St Lucia, Queensland, 4072, Australia.
Free Radic Biol Med. 2019 Apr;134:468-483. doi: 10.1016/j.freeradbiomed.2019.01.025. Epub 2019 Feb 2.
Stress is a multimodal response involving the coordination of numerous body systems in order to maximize the chance of survival. However, long term activation of the stress response results in neuronal oxidative stress via reactive oxygen and nitrogen species generation, contributing to the development of depression. Stress-induced depression shares a high comorbidity with other neurological conditions including Alzheimer's disease (AD) and dementia, often appearing as one of the earliest observable symptoms in these diseases. Furthermore, stress and/or depression appear to exacerbate cognitive impairment in the context of AD associated with dysfunctional catecholaminergic signaling. Given there are a number of homologous pathways involved in the pathophysiology of depression and AD, this article will highlight the mechanisms by which stress-induced perturbations in oxidative stress, and particularly NO signaling, contribute to neurodegeneration.
压力是一种多模态反应，涉及到许多身体系统的协调，以最大限度地提高生存的机会。然而，长期激活应激反应会导致神经元氧化应激，通过活性氧和氮物种的产生，导致抑郁的发展。应激诱导的抑郁与其他神经疾病（包括阿尔茨海默病（AD）和痴呆症）有很高的共病率，通常在这些疾病中作为最早观察到的症状之一出现。此外，在与儿茶酚胺能信号传导功能障碍相关的 AD 中，压力和/或抑郁似乎会加重认知障碍。鉴于在抑郁和 AD 的病理生理学中有许多同源途径，本文将重点介绍应激诱导的氧化应激，特别是一氧化氮信号，如何导致神经退行性变的机制。
