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Potential neuroimmunological targets in the treatment of anxiety disorders. 治疗焦虑症的潜在神经免疫学靶点。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351965
Ruihua Hou, Zhen Tang, David S Baldwin

In the translation of psychoneuroimmunology research into clinical practice, one critical step is to identify biomarkers for improved diagnosis and targeting of interventions. Inflammatory markers deserve special attention due to their crucial role linking various health conditions and disorders. In this chapter, we discuss the pivotal roles of cytokines in signalling to the brain and leading to behavioural changes. This is followed by a review of recent research findings into neuroimmunology of depression, and immunomodulating effects of antidepressants. The rest of the chapter focuses on neuroinflammatory hypothesis in anxiety disorders, and provides an overview of current research evidence on inflammatory responses in anxious state and anxiety disorders. Research suggestions are recommended, including study design, risk factors, medication effects, and measurement strategies. Clinical and pharmacotherapeutic implications and future research directions are also discussed in the final section.

在将精神神经免疫学研究转化为临床实践的过程中,一个关键步骤是确定生物标志物,以改进诊断和靶向干预。炎症标志物值得特别关注,因为它们在各种健康状况和疾病之间起着至关重要的作用。在本章中,我们讨论细胞因子在向大脑发送信号和导致行为改变中的关键作用。接下来是对抑郁症的神经免疫学和抗抑郁药的免疫调节作用的最新研究结果的回顾。本章的其余部分侧重于焦虑障碍的神经炎症假说,并概述了当前关于焦虑状态和焦虑障碍的炎症反应的研究证据。研究建议包括研究设计、危险因素、药物效果和测量策略。最后一节还讨论了临床和药物治疗意义以及未来的研究方向。
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引用次数: 6
Peripheral inflammation and cognitive aging. 外周炎症和认知老化。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000346362
Alvin Lim, Katarina Krajina, Anna L Marsland

Evidence suggests that inflammation, an innate immune response facilitating recovery from injury and pathogenic invasion, is positively associated with age-related cognitive decline and may play a role in risk for dementia. Physiological pathways linking the peripheral immune and central nervous systems are outlined, and studies linking inflammation with neurocognitive function are overviewed. We also present recent studies from our laboratory showing that midlife inflammation is related to cognitive function and brain morphology. Finally, potential implications for treatment, future directions, and limitations are discussed.

有证据表明,炎症是一种促进损伤和致病性入侵恢复的先天免疫反应,与年龄相关的认知能力下降呈正相关,并可能在痴呆风险中发挥作用。生理途径连接外周免疫和中枢神经系统概述,并研究联系炎症与神经认知功能概述。我们还介绍了我们实验室最近的研究,表明中年炎症与认知功能和大脑形态有关。最后,讨论了治疗的潜在意义、未来的发展方向和局限性。
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引用次数: 40
Basic aspects of the immunology of neuroinflammation. 神经炎症免疫学的基本方面。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343964
Eric S Wohleb, Jonathan P Godbout

Neuroinflammation is used to describe an immune-related process that occurs within the central nervous system (CNS). The objective of this chapter is to introduce basic aspects of neuroinflammation in the context of psychiatric disorders. Inflammatory processes are evident in the CNS with a myriad of stimuli including neurological disease, CNS injury or infection, peripheral infection, and psychological stress. Because the CNS maintains a degree of immune privilege, endothelial cells of the blood-brain barrier (BBB) and resident CNS innate immune cells are integral to the interpretation and propagation of inflammatory signals. For instance, activated CNS immune cells and the BBB coordinate production of cytokines and secondary messengers that act directly to influence neurophysiology. Another key concept is that there is bidirectional communication between the immune system and CNS. Afferent neuro-immune pathways relay the peripheral inflammatory profile to the CNS by secretion of cytokines and direct neuronal activation. Communication through afferent neuro-immune pathways promotes physiological and behavioral responses that are aimed to help clear pathogens from the host. For example, peripheral infection increases circulating IL-1β that induces production of prostaglandins and IL-1β by CNS immune cells that initiate fever and the behavioral symptoms of sickness. Although transient cytokine responses in the brain may be beneficial to the host, prolonged neuroinflammation associated with chronic illness, neurodegenerative disease, stress, and aging impair neuroimmune regulation and negatively affect normal cognitive and behavioral processes. Thus, understanding neuroimmune regulation and mechanisms that mediate neuroinflammation is important because these pathways likely contribute to the pathophysiology of several mental health disorders.

神经炎症被用来描述发生在中枢神经系统(CNS)内的免疫相关过程。本章的目的是在精神疾病的背景下介绍神经炎症的基本方面。在神经系统疾病、中枢神经系统损伤或感染、外周感染和心理应激等多种刺激下,炎症过程在中枢神经系统中是明显的。由于中枢神经系统保持一定程度的免疫特权,血脑屏障(BBB)内皮细胞和中枢神经系统固有免疫细胞在炎症信号的解释和传播中不可或缺。例如,激活的中枢神经系统免疫细胞和血脑屏障协调产生细胞因子和次级信使,直接影响神经生理学。另一个关键概念是免疫系统和中枢神经系统之间存在双向交流。传入神经-免疫通路通过分泌细胞因子和直接神经元激活将外周炎症传递到中枢神经系统。通过传入神经免疫途径的交流促进旨在帮助清除宿主病原体的生理和行为反应。例如,外周感染增加循环IL-1β,诱导CNS免疫细胞产生前列腺素和IL-1β,从而引发发烧和疾病的行为症状。虽然大脑中短暂的细胞因子反应可能对宿主有益,但与慢性疾病、神经退行性疾病、压力和衰老相关的长期神经炎症损害神经免疫调节,并对正常的认知和行为过程产生负面影响。因此,了解神经免疫调节和介导神经炎症的机制是重要的,因为这些途径可能有助于几种精神健康障碍的病理生理。
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引用次数: 38
Preface. 前言。
Pub Date : 2013-01-01
Angelos Halaris, Brian E Leonard
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引用次数: 0
Pharmacotherapy of posttraumatic stress disorder. 创伤后应激障碍的药物治疗。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000353540
Anthony Koller, Dan J Stein

Advances in the basic neuroscience of fear conditioning and extinction, as well as in the clinical neuroscience of posttraumatic stress disorder (PTSD), have laid the foundations for research on the pharmacotherapy of PTSD. Clinical trials have ranged from early work on tricyclic antidepressants and benzodiazepines through to more recently introduced antidepressants, and on to a range of other psychotropic agents. Despite the growing database of trials, the area remains a controversial one insofar as key systematic reviews in the field have emphasized the methodological limitations of existing work. Here, we briefly review the existing literature on the pharmacotherapy of PTSD, attempting to highlight key clinical lessons, and important areas for future research.

恐惧调节和消退基础神经科学以及创伤后应激障碍(PTSD)临床神经科学的进展,为PTSD的药物治疗研究奠定了基础。临床试验的范围从早期的三环抗抑郁药和苯二氮卓类药物到最近引入的抗抑郁药,以及一系列其他精神药物。尽管试验的数据库越来越多,但该领域仍然是一个有争议的领域,因为该领域的关键系统综述强调了现有工作的方法局限性。在此,我们简要回顾了现有的PTSD药物治疗文献,试图强调关键的临床经验教训,以及未来研究的重要领域。
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引用次数: 8
Inflammatory and oxidative and nitrosative stress cascades as new drug targets in myalgic encephalomyelitis and chronic fatigue syndrome. 炎症和氧化和亚硝化应激级联反应作为肌痛性脑脊髓炎和慢性疲劳综合征的新药物靶点。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343982
Michael Maes

Myalgic encephalomyelitis (ME), chronic fatigue syndrome (CFS) and chronic fatigue (CF) are distinct diagnostic categories with regard to clinical symptoms, severity of illness and biomarkers. Patients with ME and CFS show higher scores on fatigue, neurocognitive disorders, hyperalgesia, autonomic symptoms, postexertional malaise and a subjective feeling of infection than patients with CF. ME is characterized by increased postexertional malaise, a subjective feeling of infection and neurocognitive disorders and is a more severe variant than CFS. Fukuda's 1994 CDC criteria are adequate to make a distinction between patients with ME/CFS and CF, while ME/CFS patients should be subdivided into those with and without postexertional malaise into ME and CFS, respectively. Different interrelated pathophysiological mechanisms play a role in ME/CFS, i.e. (1) inflammation and immune activation, (2) oxidative and nitrosative stress and lowered antioxidant defenses, (3) activation of cell signaling networks, e.g. nuclear factor ĸβ, the 2 9 ,5 9 -oligoadenylate/RNase-L and/or protein kinase R pathway, (4) a transition towards autoimmune reactions, and (5) bacterial translocation. The inflammatory biomarkers are higher in ME/CFS than in CF and higher in ME than in CFS. The above-mentioned pathways may explain the onset of characteristic ME/CFS symptoms, such as fatigue, malaise, autonomic symptoms, hyperalgesia, and neurocognitive symptoms. Different etiological factors may trigger ME/CFS/CF, e.g. viral and bacterial infections, and (auto)immune and inflammatory disorders, while psychosocial and physical stressors act as modulating factors. New pathophysiologically driven drug candidates for ME and CFS are discussed which target the pathways that play a role in ME/CFS.

肌痛性脑脊髓炎(ME)、慢性疲劳综合征(CFS)和慢性疲劳(CF)在临床症状、疾病严重程度和生物标志物方面是不同的诊断类别。与CF患者相比,ME和CFS患者在疲劳、神经认知障碍、痛觉过敏、自主神经症状、运动后不适和主观感染感觉方面得分更高。ME的特征是运动后不适、主观感染感觉和神经认知障碍增加,是比CFS更严重的变体。Fukuda 1994年的CDC标准足以区分ME/CFS和CF,而ME/CFS患者应细分为有和无运动后不适的ME和CFS。不同的相关病理生理机制在ME/CFS中发挥作用,即(1)炎症和免疫激活,(2)氧化和亚硝化应激和抗氧化防御降低,(3)细胞信号网络的激活,例如核因子ĸβ, 2,9,5,9 -寡腺苷酸/RNase-L和/或蛋白激酶R途径,(4)向自身免疫反应的过渡,以及(5)细菌易位。炎症生物标志物在ME/CFS中高于CF,在ME中高于CFS。上述途径可以解释ME/CFS特征性症状的发生,如疲劳、不适、自主神经症状、痛觉过敏和神经认知症状。不同的病因可能引发ME/CFS/CF,例如病毒和细菌感染,以及(自身)免疫和炎症性疾病,而社会心理和身体压力因素是调节因素。讨论了针对ME/CFS中起作用的途径的新的病理生理驱动的ME和CFS候选药物。
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引用次数: 19
Glucocorticoids and inflammation: a double-headed sword in depression? How do neuroendocrine and inflammatory pathways interact during stress to contribute to the pathogenesis of depression? 糖皮质激素和炎症:抑郁症的双刃剑?应激时神经内分泌和炎症通路如何相互作用导致抑郁症的发病机制?
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343980
M A Horowitz, P A Zunszain, C Anacker, K Musaelyan, C M Pariante

Both glucocorticoids and inflammation have been implicated in the pathogenesis of depression. There is a large body of literature indicating that hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and glucocorticoid receptor (GR) dysfunction are present in a significant proportion of depressed patients. There is also evidence of increased inflammatory processes in depressed populations, with higher levels of cytokines being a prominent finding - including raised levels of IL-6, and IL-1. These findings appear difficult to reconcile given the well-recognised property of glucocorticoids as prominent anti-inflammatory molecules. There are three potential solutions posed to this dilemma. Firstly, it has been argued that the glucocorticoid system and the inflammatory system exist in balance with one another and chronic stress can disrupt this balance in favour of inflammatory processes at the expense of glucocorticoid signalling. It has also been suggested that glucocorticoids have more complex actions than typically thought, and, in low levels can actually be pro-inflammatory, rather than universally anti-inflammatory. Lastly, it is possible that inflammation and glucocorticoid signalling may act on the same processes and structures without direct interaction to give rise to cumulative damage. Improved understanding of this interaction will allow further progress in determining targets for treatment.

糖皮质激素和炎症都与抑郁症的发病机制有关。大量文献表明,相当比例的抑郁症患者存在下丘脑-垂体-肾上腺(HPA)轴亢进和糖皮质激素受体(GR)功能障碍。也有证据表明,抑郁人群的炎症过程增加,细胞因子水平较高是一个突出的发现,包括IL-6和IL-1水平升高。鉴于糖皮质激素作为突出的抗炎分子的公认特性,这些发现似乎难以调和。对于这一困境,有三种可能的解决方案。首先,有人认为糖皮质激素系统和炎症系统彼此平衡存在,慢性应激会破坏这种平衡,以糖皮质激素信号传导为代价,有利于炎症过程。也有人认为,糖皮质激素的作用比通常认为的要复杂得多,而且,低水平的糖皮质激素实际上可以促炎,而不是普遍的抗炎。最后,炎症和糖皮质激素信号可能作用于相同的过程和结构,但没有直接相互作用,从而导致累积损伤。对这种相互作用的更好理解将有助于在确定治疗目标方面取得进一步进展。
{"title":"Glucocorticoids and inflammation: a double-headed sword in depression? How do neuroendocrine and inflammatory pathways interact during stress to contribute to the pathogenesis of depression?","authors":"M A Horowitz,&nbsp;P A Zunszain,&nbsp;C Anacker,&nbsp;K Musaelyan,&nbsp;C M Pariante","doi":"10.1159/000343980","DOIUrl":"https://doi.org/10.1159/000343980","url":null,"abstract":"<p><p>Both glucocorticoids and inflammation have been implicated in the pathogenesis of depression. There is a large body of literature indicating that hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis and glucocorticoid receptor (GR) dysfunction are present in a significant proportion of depressed patients. There is also evidence of increased inflammatory processes in depressed populations, with higher levels of cytokines being a prominent finding - including raised levels of IL-6, and IL-1. These findings appear difficult to reconcile given the well-recognised property of glucocorticoids as prominent anti-inflammatory molecules. There are three potential solutions posed to this dilemma. Firstly, it has been argued that the glucocorticoid system and the inflammatory system exist in balance with one another and chronic stress can disrupt this balance in favour of inflammatory processes at the expense of glucocorticoid signalling. It has also been suggested that glucocorticoids have more complex actions than typically thought, and, in low levels can actually be pro-inflammatory, rather than universally anti-inflammatory. Lastly, it is possible that inflammation and glucocorticoid signalling may act on the same processes and structures without direct interaction to give rise to cumulative damage. Improved understanding of this interaction will allow further progress in determining targets for treatment. </p>","PeriodicalId":74212,"journal":{"name":"Modern trends in pharmacopsychiatry","volume":"28 ","pages":"127-43"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000343980","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32671379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 51
The early phases of anxiety disorders: from prevention to treatment. 焦虑症的早期阶段:从预防到治疗。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000351931
Javier Vázquez-Bourgon, Andres Herrán, José Luis Vázquez-Barquero

The 'early intervention' model has been applied with good results to the care of a range of serious medical conditions. The key rationale for this model is to guarantee early identification and treatment for the illness, thus preventing its progression to a more advanced and severe stage. It would also provide a framework for optimal treatment according to the stage of the disorders. Although in the field of psychiatry this model has mainly been implemented in nonaffective psychosis, research evidence supports its application in other mental disorders. To promote this initiative, the chapter explores the available evidence demonstrating the feasibility of adopting the key elements of the model in the care of the whole spectrum of anxiety disorders. In addition, the chapter describes the different stages that are possible to identify in the process of developing an illness, and also the phase-specific interventions that could be applied. Finally, the service repercussions of implementing an early intervention model in anxiety disorders are discussed.

"早期干预"模式已被应用于一系列严重医疗状况的护理,并取得了良好的效果。这种模式的关键原理是保证疾病的早期识别和治疗,从而防止其发展到更高级和更严重的阶段。它还将根据疾病的阶段提供最佳治疗的框架。尽管在精神病学领域,该模型主要应用于非情感性精神病,但研究证据支持其在其他精神障碍中的应用。为了促进这一倡议,本章探讨了现有的证据,证明在整个焦虑障碍的护理中采用该模型的关键要素的可行性。此外,本章还描述了在疾病发展过程中可能确定的不同阶段,以及可以应用的具体阶段干预措施。最后,讨论了在焦虑障碍中实施早期干预模式的服务效果。
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引用次数: 2
Evidence-based treatment pathways for translational studies in obsessive-compulsive disorders. 强迫症转化研究的循证治疗途径。
Pub Date : 2013-01-01 Epub Date: 2013-09-20 DOI: 10.1159/000353618
N A Fineberg, S Pallanti, S Reghunandanan

Obsessive-compulsive disorder (OCD) and related disorders are costly and burdensome long-term illnesses. Whilst evidence-based pharmacological and psychological treatments are available for OCD, a significant proportion of OCD patients fail to respond and for many of the OCD-related disorders no validated treatments are as yet recognised. In addition, predictors of treatment response/non-response to guide clinicians in the management of individual patients are lacking. The introduction of personalised medicine to psychiatry is expected to offer the novel prospect of identifying the most effective treatment for a patient in a timely and cost-effective way. Translational research that investigates endophenotype predictors of treatment response in OCD and related disorders may pave the way toward personalised medicine. Such research is likely to require multidisciplinary collaboration between neuroscientists and clinicians, so that the right clinical questions are addressed, and large datasets, entailing multinational, multicentre sampling. In order to facilitate the translational investigation of the key aspects of the treatment response, these studies would require access to standardised treatment paradigms that are internationally recognised. In this chapter, we introduce some of the most important outstanding questions for personalised medicine that translational research could be expected to address within the next 10 years. We review the available tools and techniques for standardised clinical assessment and the criteria that are used to define the degree of therapeutic response (response, remission, relapse, resistance) that would naturally dictate the direction of treatment. We also present a series of consecutive stepped treatment algorithms based on evidence-based practice and modelled on naturalistic care that we believe could be adapted to multicentre settings as a template for the translational researcher to aid in the design of pragmatic treatment trials that are capable of identifying biomarkers of treatment response or non-response at each key stage of the evidence-based canon.

强迫症(OCD)及相关疾病是一种代价高昂、负担沉重的长期疾病。虽然基于证据的药理学和心理学治疗方法可用于强迫症,但很大一部分强迫症患者没有反应,而且对于许多强迫症相关疾病,尚未发现有效的治疗方法。此外,缺乏治疗反应/无反应的预测指标来指导临床医生对个体患者的管理。精神病学个体化治疗的引入有望提供一种新的前景,即以及时和经济有效的方式为患者确定最有效的治疗方法。研究强迫症和相关疾病治疗反应的内表型预测因子的转化研究可能为个性化医疗铺平道路。这样的研究可能需要神经科学家和临床医生之间的多学科合作,以便解决正确的临床问题,以及需要多国、多中心采样的大型数据集。为了促进对治疗反应关键方面的转化研究,这些研究将需要获得国际公认的标准化治疗范例。在本章中,我们介绍了一些最重要的个性化医疗的突出问题,这些问题有望在未来10年内得到转化研究的解决。我们回顾了用于标准化临床评估的可用工具和技术,以及用于定义治疗反应程度(反应、缓解、复发、抵抗)的标准,这些标准自然地决定了治疗的方向。我们还提出了一系列基于循证实践的连续阶梯治疗算法,并以自然护理为模型,我们认为这些算法可以适应多中心环境,作为翻译研究人员的模板,以帮助设计实用的治疗试验,这些试验能够在循证经典的每个关键阶段识别治疗反应或无反应的生物标志物。
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引用次数: 2
Inflammation as the cause of the metabolic syndrome in depression. 炎症作为抑郁症代谢综合征的病因。
Pub Date : 2013-01-01 Epub Date: 2013-02-27 DOI: 10.1159/000343974
Brian E Leonard

Physical ill-health is a common feature of depression. Cardiovascular disease, type 2 diabetes and cancer are, for example, common occurrences and lead to increased morbidity and mortality. The question arises whether these changes are attributable to an unhealthy life style or due to genetic or other causes that are exacerbated by stress and adverse environmental factors. Of the various factors which have been implicated, chronic low-grade inflammation has received much attention in recent years. For this reason, the following review assesses the evidence that implicates inflammation in the psychopathology of major depression and how this is linked to the increased incidence of physical illness in these patients.

身体不健康是抑郁症的一个共同特征。例如,心血管疾病、2型糖尿病和癌症是常见病,并导致发病率和死亡率增加。问题是,这些变化是由于不健康的生活方式,还是由于遗传或其他原因,而压力和不利的环境因素又加剧了这些原因。在涉及的各种因素中,慢性低度炎症近年来受到了广泛的关注。出于这个原因,下面的综述评估了炎症与重度抑郁症的精神病理相关的证据,以及炎症与这些患者身体疾病发病率增加的关系。
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引用次数: 24
期刊
Modern trends in pharmacopsychiatry
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