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神经炎症相关的大脑改变作为焦虑障碍的潜在神经生物标志物。

Neuroinflammation-Associated Alterations of the Brain as Potential Neural Biomarkers in Anxiety Disorders.

机构信息

Department of Psychiatry, CHA Bundang Medical Center, CHA University, Seongnam 13496, Korea.

Department of Psychiatry, Korea University Ansan Hospital, Korea University College of Medicine, Ansan 15355, Korea.

出版信息

Int J Mol Sci. 2020 Sep 7;21(18):6546. doi: 10.3390/ijms21186546.

DOI:10.3390/ijms21186546
PMID:32906843
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7555994/
Abstract

Stress-induced changes in the immune system, which lead to neuroinflammation and consequent brain alterations, have been suggested as possible neurobiological substrates of anxiety disorders, with previous literature predominantly focusing on panic disorder, agoraphobia, and generalized anxiety disorder, among the anxiety disorders. Anxiety disorders have frequently been associated with chronic stress, with chronically stressful situations being reported to precipitate the onset of anxiety disorders. Also, chronic stress has been reported to lead to hypothalamic-pituitary-adrenal axis and autonomic nervous system disruption, which may in turn induce systemic proinflammatory conditions. Preliminary evidence suggests anxiety disorders are also associated with increased inflammation. Systemic inflammation can access the brain, and enhance pro-inflammatory cytokine levels that have been shown to precipitate direct and indirect neurotoxic effects. Prefrontal and limbic structures are widely reported to be influenced by neuroinflammatory conditions. In concordance with these findings, various imaging studies on panic disorder, agoraphobia, and generalized anxiety disorder have reported alterations in structure, function, and connectivity of prefrontal and limbic structures. Further research is needed on the use of inflammatory markers and brain imaging in the early diagnosis of anxiety disorders, along with the possible efficacy of anti-inflammatory interventions on the prevention and treatment of anxiety disorders.

摘要

压力导致免疫系统发生变化,从而引发神经炎症和随后的大脑改变,这被认为是焦虑障碍的可能神经生物学基础,先前的文献主要集中在焦虑障碍中的恐慌症、广场恐惧症和广泛性焦虑症。焦虑障碍常与慢性压力有关,据报道,慢性压力环境会引发焦虑障碍的发作。此外,慢性压力已被报道会导致下丘脑-垂体-肾上腺轴和自主神经系统紊乱,这可能反过来导致全身促炎状态。初步证据表明,焦虑障碍也与炎症增加有关。全身炎症可以进入大脑,并增强促炎细胞因子水平,这些细胞因子已被证明会引发直接和间接的神经毒性作用。广泛报道称,前额叶和边缘结构受到神经炎症状态的影响。与这些发现一致,对恐慌症、广场恐惧症和广泛性焦虑症的各种影像学研究报告称,前额叶和边缘结构的结构、功能和连接发生了改变。需要进一步研究炎症标志物和大脑成像在焦虑障碍早期诊断中的应用,以及抗炎干预对预防和治疗焦虑障碍的可能疗效。

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