Neurobiology of Stress最新文献

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Gut Microbiome-Liver-Brain axis in Alcohol Use Disorder. The role of gut dysbiosis and stress in alcohol-related cognitive impairment progression: possible therapeutic approaches 酒精使用障碍中的肠道微生物群-肝-脑轴。肠道生态失调和应激在酒精相关认知障碍进展中的作用：可能的治疗方法

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-02-08 DOI: 10.1016/j.ynstr.2025.100713

Emilio Merlo Pich , Ioannis Tarnanas , Patrizia Brigidi , Ginetta Collo

The Gut Microbiome-Liver-Brain Axis is a relatively novel construct with promising potential to enhance our understanding of Alcohol Use Disorder (AUD), and its therapeutic approaches. Significant alterations in the gut microbiome occur in AUD even before any other systemic signs or symptoms manifest. Prolonged and inappropriate alcohol consumption, by affecting the gut microbiota and gut mucosa permeability, is thought to contribute to the development of behavioral and cognitive impairments, leading to Alcohol-Related Liver Disorders and potentially progressing into alcoholic cirrhosis, which is often associated with severe cognitive impairment related to neurodegeneration, such as hepatic encephalopathy and alcoholic dementia.

The critical role of the gut microbiota is further supported by the efficacy of FDA-approved treatments for hepatic encephalopathy in alcoholic cirrhosis (i.e., lactulose and rifaximin). To stimulate new research, we hypothesize that interactions between a maladaptive stress response and a constitutional predisposition to neurodegeneration underlie the progression of AUD to conditions of Alcohol-Related Clinical Concerns with severe cognitive impairment, which represent a significant and costly burden to society. Early identification of AUD individuals at risk for developing these conditions could help to prioritize integrated therapeutic interventions targeting different substrates of the Gut Microbiome-Liver-Brain axis. Specifically, addiction medications, microbiome modulators, stress-reducing interventions, and, possibly soon, novel agents that reduce hepatic steatosis/fibrosis will be discussed in the context of digitally supported integrated therapeutic approaches. The explicit goal of this AUD treatment performed on the early stage of the disorder would be to reduce the transition from AUD to those conditions of Alcohol-Related Common Clinical Concerns associated with severe cognitive impairment, a strategy recommended for most neurological neurodegenerative disorders.

肠道微生物组-肝-脑轴是一个相对较新的结构，有希望增强我们对酒精使用障碍（AUD）及其治疗方法的理解。AUD患者肠道微生物组的显著改变甚至在任何其他系统性体征或症状出现之前就已发生。长期和不适当的饮酒，通过影响肠道微生物群和肠道粘膜通透性，被认为有助于行为和认知障碍的发展，导致酒精相关性肝病，并可能发展为酒精性肝硬化，这通常与与神经变性相关的严重认知障碍有关，如肝性脑病和酒精性痴呆。fda批准的治疗酒精性肝硬化肝性脑病（即乳果糖和利福昔明）的疗效进一步支持了肠道微生物群的关键作用。为了刺激新的研究，我们假设，适应不良的应激反应和神经变性体质易感之间的相互作用是AUD发展为酒精相关临床问题的基础，并伴有严重的认知障碍，这对社会来说是一个重大而昂贵的负担。早期识别有发展这些疾病风险的AUD个体可以帮助优先考虑针对肠道微生物群-肝-脑轴不同底物的综合治疗干预。具体来说，成瘾药物、微生物组调节剂、减压干预，以及可能很快就会出现的减少肝脂肪变性/纤维化的新型药物，将在数字支持的综合治疗方法的背景下进行讨论。在疾病早期进行AUD治疗的明确目标是减少AUD向与严重认知障碍相关的酒精相关常见临床问题的过渡，这是大多数神经退行性疾病推荐的策略。

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Illuminating the impact of stress: In vivo approaches to track stress-related neural adaptations 阐明压力的影响：体内方法跟踪压力相关的神经适应

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-02-07 DOI: 10.1016/j.ynstr.2025.100712

Puja K. Parekh

Stressful experiences can affect both daily life and long-term health outcomes in a variety of ways. Acute challenges may be adaptive, promoting arousal and enhancing memory and cognitive function. Importantly, however, chronic stress dysregulates the body's physiological regulatory mechanisms consisting of complex hormone interactions throughout the peripheral and central nervous systems. This disrupted signaling consequently alters the balance of synapse formation, maturation and pruning, processes which regulate neural communication, plasticity, learning, cognitive flexibility and adaptive behaviors - hallmarks of a healthy, functional brain. The chronically stressed brain state, therefore, is one which may be uniquely vulnerable. To understand the development of this state, how it is sustained and how behavior and neural function are transiently or indelibly impacted by it, we can turn to a number of advanced approaches in animal models which offer unprecedented insights. This has been the aim of my recent work within the field and the goal of my new independent research program. To achieve this, I have employed methods to uncover how key brain circuits integrate information to support motivated behaviors, how stress impacts their ability to perform this process and how best to operationalize behavioral readouts. Here I present an overview of research contributions that I find most meaningful for advancing our understanding of the impact of stress and propose new avenues which will guide my own framework to address the salient outstanding questions within the field.

压力经历会以各种方式影响日常生活和长期健康结果。急性挑战可能是适应性的，促进觉醒，增强记忆和认知功能。然而，重要的是，慢性应激失调了身体的生理调节机制，包括整个外周和中枢神经系统中复杂的激素相互作用。这种中断的信号最终改变了突触形成、成熟和修剪的平衡，这些过程调节神经通信、可塑性、学习、认知灵活性和适应性行为——这是健康、功能性大脑的标志。因此，长期受到压力的大脑状态可能是一种特别脆弱的状态。为了理解这种状态的发展，它是如何持续的，以及行为和神经功能如何受到它的短暂或不可磨灭的影响，我们可以求助于动物模型中的一些先进方法，这些方法提供了前所未有的见解。这是我最近在该领域工作的目的，也是我新的独立研究计划的目标。为了实现这一目标，我采用了一些方法来揭示关键的大脑回路是如何整合信息来支持动机行为的，压力是如何影响他们执行这一过程的能力的，以及如何最好地操作行为读数。在这里，我概述了我认为对推进我们对压力影响的理解最有意义的研究贡献，并提出了新的途径，这些途径将指导我自己的框架来解决该领域内突出的突出问题。

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The zona incerta regulates burying behavior and normalizes anxiety-like behavior in inescapable stressful male mice by object cue 无虫带通过物体提示调节不可逃避的应激雄性小鼠的埋藏行为和使焦虑样行为正常化

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01 DOI: 10.1016/j.ynstr.2024.100704

Yueqin Liu , Lianli Qiu , Jiahui Qian , Qiang Xu , Rongfeng Qi , Yifeng Luo , Zhihong Cao , Zhiqiang Zhang , Wei Wu , Longjiang Zhang , Guangming Lu

Inescapable stressful events often precipitate long-term alterations in emotion-related behaviors and poor sleep quality, with anxiety being a prevalent associated disorder. The defensive burying behavior of rodents is a response to imminent threats that becomes markedly pronounced in response to anxiety. However, the neural foundations of defensive burying behavior and etiology of anxiety remain largely unknown. In this study, we established a model employing object binding to elicit increased burying behavior in mice, thereby enhancing fear resolution and subsequently reducing anxious behaviors. Notably, the mice that associated shock with an object exhibited less object exploration and the zona incerta (ZI) neurons showed higher calcium activity during object exploration as compared to the Shock only mice. Although the calcium activity in ZI neurons of the Object mice was identical to the Shock only mice, the Object mice exhibited more burying behavior. Furthermore, the time spent in the center of the open-field test was directly proportional to the duration of burying behavior. Chemogenetic activation of ZI neurons extended the burying time and concomitantly ameliorated anxiety-like behavior. Importantly, chemogenetic enhancement of projection from ZI neurons to the ventral periaqueductal gray (vPAG), a brain region that plays a critical role in autonomic function, normalizes anxious behavior without influencing burying behavior. Collectively, these findings systematically reveal the functions and underlying mechanisms of the ZI-vPAG circuit in controlling behaviors akin to anxiety, offering significant insights into ZI's role in the pathophysiology of anxiety disorders.

不可避免的压力事件往往会导致情绪相关行为的长期改变和睡眠质量下降，焦虑是一种普遍的相关障碍。啮齿动物的防御性掩埋行为是对迫在眉睫的威胁的一种反应，在焦虑的反应中变得明显。然而，防御性埋藏行为的神经基础和焦虑的病因学在很大程度上仍然未知。在这项研究中，我们建立了一个模型，利用物体绑定来引发小鼠增加的埋藏行为，从而增强恐惧解决，从而减少焦虑行为。值得注意的是，与只有电击的小鼠相比，将电击与物体联系起来的小鼠表现出较少的物体探索，并且在物体探索过程中，无动带（ZI）神经元显示出更高的钙活性。虽然Object小鼠的ZI神经元钙活性与电击小鼠相同，但Object小鼠表现出更多的埋藏行为。此外，在空地试验中心停留的时间与掩埋行为的持续时间成正比。ZI神经元的化学发生激活延长了掩埋时间，并随之改善了焦虑样行为。重要的是，从ZI神经元到腹侧导水管周围灰质（vPAG）（一个在自主神经功能中起关键作用的大脑区域）的投射的化学发生增强使焦虑行为正常化，而不影响掩埋行为。总的来说，这些发现系统地揭示了ZI- vpag回路在控制类似焦虑的行为中的功能和潜在机制，为ZI在焦虑障碍的病理生理学中的作用提供了重要的见解。

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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IF 3.6 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01

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Shared genetic risk and causal associations between Post-traumatic stress disorder and migraine with antithrombotic agents and other medications 抗血栓药物和其他药物在创伤后应激障碍和偏头痛之间的共同遗传风险和因果关系。

IF 4.3 2区医学 Q1 NEUROSCIENCES

Neurobiology of Stress

Pub Date : 2025-01-01 DOI: 10.1016/j.ynstr.2024.100703

Charlotte K. Bainomugisa , The International Headache Genetics Consortium (IHGC), Dagmar Bruenig , Heidi G. Sutherland , Lyn R. Griffiths , Dale R. Nyholt , Divya Mehta

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that frequently co-occurs with pain disorders including migraine. There are proposed biological, genetic and environmental factors associated with both PTSD and migraine suggesting shared etiology. Genome-Wide Association Studies (GWAS) have been used to identify genomic risk loci associated with various disorders and to investigate genetic overlap between traits. There is a significant genetic correlation between PTSD and migraine with no evidence of a causal relationship that could be attributed to pleiotropy. Cross-disorder genetic analyses were applied to investigate the genetic overlap and causal associations using GWAS summary statistics of PTSD (n = 214408), migraine (n = 873341) and 23 medication use traits (n = 78808–305913) including anti-depressants, anti-migraine preparations and beta-blocking agents.

Across the entire genome, anti-thrombotic agents had a significant and negative genetic correlation with PTSD (rG = −0.2, P_FDR = 0.032) and a positive genetic correlation with migraine (rG = 0.26, P_FDR = 2.23 x 10⁻⁸). PTSD showed significant genetic correlation with 11 other medication use traits including beta blocking agents (rG = −0.11, P_FDR = 0.034). Of the 2495 genomic regions tested, PTSD showed significant local genetic correlation with 12 medication use traits at 43 loci; while migraine showed significant genetic correlation with only anti-inflammatory agents and anti-rheumatic products at locus 12:57522282–57607142 (DAB1) (P < 2 x 10⁻⁵). The genetic liability to PTSD had a causal effect on increased risk of using pain medication such as opioids (β_ivw = 0.59, P = 5.21 x 10⁻⁵) while the genetic liability to migraine had a causal effect on the increased risk of using anti-thrombotic agents (β_ivw = 0.59, P = 1.69 x 10⁻⁷). The genes in the genomic regions shared between PTSD and medication use traits were enriched in neural-related pathways such as neuron development, neurogenesis and protein kinase activity. These results provide further insight into the genetically controlled biological and environmental factors underlying the shared etiology between PTSD and migraine. The identified biomarkers can be used as a basis for investigation as potential drug targets for both disorders. These findings are significant for drug re-purposing and treatment of PTSD and migraine using monotherapy.

创伤后应激障碍（PTSD）是一种精神障碍，经常与偏头痛等疼痛障碍共同发生。目前提出的生物、遗传和环境因素与创伤后应激障碍和偏头痛有关，这表明它们有共同的病因。全基因组关联研究（GWAS）已被用于识别与各种疾病相关的基因组风险位点，并研究性状之间的遗传重叠。创伤后应激障碍和偏头痛之间存在显著的遗传相关性，但没有证据表明其与多效性之间存在因果关系。交叉障碍遗传分析应用GWAS汇总统计研究PTSD （n = 214408）、偏头痛（n = 873341）和23种药物使用特征（n = 78808-305913）（包括抗抑郁药、抗偏头痛制剂和β -阻滞剂）的遗传重叠和因果关系。在整个基因组中，抗血栓药物与PTSD具有显著的负遗传相关性（rG = -0.2, P FDR = 0.032），与偏头痛具有正遗传相关性（rG = 0.26, P FDR = 2.23 × 10-8）。PTSD与包括阻断剂在内的其他11种药物使用特征具有显著的遗传相关性（rG = -0.11, P FDR = 0.034）。在测试的2495个基因组区域中，PTSD与43个位点的12个药物使用特征显示出显著的局部遗传相关性；而偏头痛仅与抗炎药和抗风湿药物在基因座12:57522282-57607142 (DAB1) （P -5）有显著的遗传相关性。PTSD遗传倾向与阿片类药物使用风险增加有因果关系（β ivw = 0.59, P = 5.21 x 10-5），偏头痛遗传倾向与抗血栓药物使用风险增加有因果关系（β ivw = 0.59, P = 1.69 x 10-7）。在创伤后应激障碍和药物使用特征之间共享的基因组区域中，基因在神经元发育、神经发生和蛋白激酶活性等神经相关途径中富集。这些结果为PTSD和偏头痛之间共同病因的遗传控制的生物和环境因素提供了进一步的见解。鉴定的生物标志物可作为研究这两种疾病的潜在药物靶点的基础。这些发现对药物再利用和使用单一疗法治疗PTSD和偏头痛具有重要意义。

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