Biomarkers in Neuropsychiatry最新文献_第2页

A systematic review of in vivo brain insulin resistance biomarkers in humans 人体内脑胰岛素抵抗生物标志物的系统综述

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-03-08 DOI: 10.1016/j.bionps.2025.100125

Graham Reid , Brendan Sargent , Sarah Bauermeister , Amanda Adler , Ivan Koychev

Type 2 diabetes mellitus (T2DM) is associated with an elevated risk of dementia, prompting interest into the concept of brain-specific insulin resistance. However, the brain's reliance on insulin-independent glucose transporters complicates attempts to measure in vivo brain insulin resistance using the definition of system-wide insulin resistance, which is based on glucose-insulin interactions. In this review, we explore three available biomarkers for evaluating in vivo brain-specific insulin resistance in humans: (1) correlating systemic insulin resistance with brain function, (2) examining functional brain changes after the administration of intranasal insulin, and (3) quantifying insulin signalling proteins in neuronally enriched blood-derived extracellular vesicles. Integrating evidence from these three approaches tentatively suggests for the first time that a comprehensive assessment of the brain's default mode network (DMN), combining these methodologies within a single study, may offer a useful biomarker to quantify in vivo brain-specific insulin resistance in humans. Correlating DMN responses to concentrations of pY-IRS-1 in blood-derived extracellular vesicles would corroborate evidence for a brain-specific biomarker and provide a scalable approach to detecting brain-specific insulin resistance in humans. This advancement would enable in vivo evaluations of insulin resistance in the central nervous system, akin to the precise measurements of systemic insulin resistance seen in T2DM. An established and clearly defined biomarker of in vivo brain insulin resistance in humans would permit further investigation into the links between diabetes and dementia, ultimately bolstering support for secondary dementia prevention by identifying those at higher risk for cognitive decline.

2型糖尿病（T2DM）与痴呆风险升高相关，促使人们对脑特异性胰岛素抵抗的概念产生兴趣。然而，大脑对胰岛素不依赖型葡萄糖转运体的依赖使得使用基于葡萄糖-胰岛素相互作用的全系统胰岛素抵抗的定义来测量体内大脑胰岛素抵抗的尝试变得复杂。在这篇综述中，我们探索了三种可用的生物标志物来评估人类体内脑特异性胰岛素抵抗：(1)全身胰岛素抵抗与脑功能的相关性；(2)检测鼻内胰岛素给药后脑功能的变化；(3)量化神经元丰富的血源性细胞外囊泡中的胰岛素信号蛋白。综合这三种方法的证据，首次初步表明，在一项研究中结合这些方法，对大脑默认模式网络（DMN）进行全面评估，可能为量化人类体内脑特异性胰岛素抵抗提供有用的生物标志物。将DMN反应与血液来源的细胞外囊泡中pY-IRS-1的浓度相关联，将证实脑特异性生物标志物的存在，并为检测人类脑特异性胰岛素抵抗提供一种可扩展的方法。这一进展将使中枢神经系统胰岛素抵抗的体内评估成为可能，类似于在T2DM中看到的全身胰岛素抵抗的精确测量。人类体内脑胰岛素抵抗的生物标志物的建立和明确定义将允许进一步研究糖尿病和痴呆之间的联系，最终通过识别认知能力下降风险较高的人来支持继发性痴呆的预防。

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Whole-body hyperthermia as a novel antidepressant therapy 全身热疗作为一种新的抗抑郁疗法

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-03-04 DOI: 10.1016/j.bionps.2025.100124

Kevin D. Gaitonde , Henry A. Nasrallah

First-line treatments for major depressive disorder include medication and cognitive behavioral therapy. While effective, pharmacotherapy often takes time to start demonstrating efficacy in symptomatic improvement and may be accompanied by adverse effects, indicating an ongoing need for new therapeutic approaches. A recently emerging somatic antidepressant intervention is whole-body hyperthermia, in which subjects are temporarily exposed to heat and then allowed to cool down. Recent studies employing hyperthermia-based strategies appear to show mood improvements both immediately and several weeks after the conclusion of treatment. However, published studies are often limited by their sample sizes and by their selection criteria. In this article, we review the literature on this novel approach and propose ideas regarding the possible physiological basis of this novel intervention and how it may be used in the future as adjunctive therapy with the current standard of care.

重度抑郁症的一线治疗包括药物治疗和认知行为治疗。药物治疗虽然有效，但往往需要一段时间才能开始显示对症状改善的疗效，并可能伴有不良反应，这表明需要持续寻找新的治疗方法。最近出现的一种身体抗抑郁干预是全身热疗，在这种治疗中，受试者暂时暴露在高温下，然后让其降温。最近的研究采用了基于热疗的策略，似乎显示了情绪的立即改善和治疗结束后的几周。然而，已发表的研究往往受到样本量和选择标准的限制。在这篇文章中，我们回顾了关于这种新方法的文献，并就这种新干预的可能生理基础提出了一些想法，以及它如何在未来作为辅助治疗与当前的护理标准一起使用。

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Inducible HSP72 protein as a marker of neuronal vulnerability in brain research: A potential biomarker for clinical psychiatry? 诱导型HSP72蛋白作为脑研究中神经元易损性的标志物：临床精神病学的潜在生物标志物？

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-02-08 DOI: 10.1016/j.bionps.2025.100123

Ana-Maria Iorgu , Dragos Inta , Peter Gass

The aim of this review is to analyze the potential of the inducible form of 70-kDa heat shock protein (i.e. HSP72) as a biomarker for neuropsychiatric diseases, focusing on both animal and clinical studies. We first discuss findings from animal studies where HSP72 has already revealed its reliability as a sensitive marker of neuronal vulnerability, especially research investigating NMDAR antagonists-induced neurotoxicity, cerebral ischemia, epilepsy, behavioral stress, and effects of psychoactive and/or addictive substances. Next, we summarized human studies providing evidence for the involvement of HSP72 in the pathology of neuropsychiatric disorders like major depression, bipolar disorder, schizophrenia, attention deficit hyperactivity disorder, autism spectrum disorder, and neurodegenerative disorders. Finally, we discuss potential future research approaches needed to further investigate and possibly validate HSP72 as a biomarker in clinical psychiatry.

本综述的目的是分析70 kda热休克蛋白（即HSP72）的诱导形式作为神经精神疾病的生物标志物的潜力，重点是动物和临床研究。我们首先讨论来自动物研究的发现，其中HSP72已经揭示了其作为神经元易感性标志物的可靠性，特别是研究NMDAR拮抗剂诱导的神经毒性、脑缺血、癫痫、行为应激以及精神活性和/或成瘾物质的影响。接下来，我们总结了HSP72参与神经精神疾病病理的人类研究，如重度抑郁症、双相情感障碍、精神分裂症、注意缺陷多动障碍、自闭症谱系障碍和神经退行性疾病。最后，我们讨论了潜在的未来研究方法，需要进一步调查和可能验证HSP72作为临床精神病学的生物标志物。

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Is low-grade inflammation related to cognitive performance during a sustained attention task in depression? – A case-control study 轻度炎症是否与抑郁症患者持续注意力任务中的认知表现有关？-病例对照研究

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-02-06 DOI: 10.1016/j.bionps.2025.100121

Bruno Pedraz-Petrozzi , Eva Kathrin Lamadé , Nils Mischa Hübner , Jil Zippelius , Elena Neumann , Gebhard Sammer

This study aimed to investigate the associations between inflammatory cytokines and cognitive performance in individuals with depression compared to healthy controls, while accounting for variables, such as perceived fatigue, BMI, and age. Individuals diagnosed with depression (n = 23) and healthy controls (n = 31) were included in the study. A 15-minute sustained attention task (subtest of the Test Battery for Attention, version 2.3.1) was administered with concurrent electroencephalographic recordings to evaluate P300 amplitude and latency. Peripheral inflammation was assessed by measuring IL-6, IL-1β, and TNF-α levels. Perceived fatigue was assessed using the German version of the Fatigue Impact Scale. Generalized linear models (GLM) were used to evaluate the main aims of the study. Results indicated that depression was associated with reduced P300 amplitudes (p = 0.011), and age was significantly associated with P300 amplitude, with older participants showing reductions (p = 0.016). However, no significant effects of inflammatory markers on P300 components were found. While no group differences were observed in the total number of hits, both perceived fatigue (p = 0.033) and TNF-α (p = 0.007) were significantly associated with hit accuracy. A post-hoc mediation analysis explored that perceived fatigue mediates the relationship between depression and number of hits. These findings suggest that low-grade inflammation may not directly influence P300 components, though inflammation and fatigue appear linked to accuracy deficits. Finally, the impact of depression on the number of hits is primarily mediated by perceived fatigue, suggesting that fatigue is a crucial factor in how depression affects cognition.

这项研究旨在调查炎症细胞因子与抑郁症患者认知表现之间的关系，同时考虑到感知疲劳、体重指数和年龄等变量。被诊断为抑郁症的个体（n = 23）和健康对照（n = 31）被纳入研究。进行15分钟持续注意任务（2.3.1版注意测试电池的子测试），同时进行脑电图记录，以评估P300振幅和潜伏期。通过测量IL-6、IL-1β和TNF-α水平来评估外周炎症。感知疲劳使用德语版疲劳影响量表进行评估。使用广义线性模型（GLM）来评估研究的主要目的。结果表明，抑郁与P300波幅降低相关（p = 0.011），年龄与P300波幅显著相关，年龄越大的参与者P300波幅降低（p = 0.016）。然而，没有发现炎症标志物对P300成分的显著影响。虽然在总命中数上没有观察到组间差异，但感知疲劳（p = 0.033）和TNF-α （p = 0.007）与命中准确性显著相关。一项事后中介分析探讨了感知疲劳在抑郁和命中次数之间的中介关系。这些发现表明，尽管炎症和疲劳似乎与准确性缺陷有关，但低度炎症可能不会直接影响P300成分。最后，抑郁对击球次数的影响主要是由感知疲劳介导的，这表明疲劳是抑郁如何影响认知的关键因素。

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Advancing transdiagnostic data analytics using knowledge graphs 利用知识图谱推进跨诊断数据分析

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-02-01 DOI: 10.1016/j.bionps.2025.100122

Fiona Klaassen , Emanuel Schwarz

Artificial intelligence approaches have tremendous potential to advance our understanding of biological and other processes contributing to mental illness risk. An important question is how such approaches can be tailored to support transdiagnostic investigations that are considered central for gaining deeper insight into etiological processes and psychopathology that may not align well with categorical illness delineations. Here, we present the so-called “knowledge graphs” that could be leveraged in analytic approaches to synthesize multimodal data of transdiagnostic relevance, identify important latent structures and biomarkers, and support the evaluation of existing transdiagnostic frameworks.

人工智能方法具有巨大的潜力，可以促进我们对导致精神疾病风险的生物和其他过程的理解。一个重要的问题是如何调整这些方法来支持跨诊断调查，这些调查被认为是获得更深入了解病因过程和精神病理学的核心，这些过程和精神病理学可能与分类疾病描述不太一致。在这里，我们提出了所谓的“知识图谱”，可以在分析方法中利用它来综合多模态的跨诊断相关性数据，识别重要的潜在结构和生物标志物，并支持对现有跨诊断框架的评估。

引用次数: 0

Biomarkers in alcohol use disorder - The promise and pitfalls of neuroimaging drug cue reactivity 酒精使用障碍的生物标志物——神经成像药物线索反应的前景和缺陷

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-01-29 DOI: 10.1016/j.bionps.2025.100119

Marlen Pfisterer , Sina Zimmermann , Judith Zaiser , Sarah Gerhardt , Sabine Vollstädt-Klein , Falk Kiefer , Patrick Bach

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Developing non-invasive molecular markers for early risk assessment of Alzheimer's disease 开发用于阿尔茨海默病早期风险评估的非侵入性分子标记

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2025-01-28 DOI: 10.1016/j.bionps.2025.100120

Tapas K. Sur , Tanmoy Mondal , Zarish Noreen , Jheannelle Johnson , Gail Nunlee-Bland , Christopher A. Loffredo , Brent E. Korba , Vijay Chandra , Siddhartha S. Jana , Bernard Kwabi-Addo , Sumit Sarkar , Somiranjan Ghosh

Alzheimer's disease (AD) is a heterogeneous neurodegenerative disease, with no standard biomarker(s) to detect or confirm its risk at an early stage. The prevalence of AD increases exponentially worldwide in people of ages over 65 and older. Current improvements have unveiled the disease's pathophysiology and clinical diagnostic tests, targeting the neurological changes (neurodegeneration, amyloid precursor protein metabolism and tangle pathology) with precise PET/MRI imaging and xMAP/SIMOA (Multiplex simultaneous detection/single molecule array) to identify and quantify β-amyloids (Aβ40, Aβ42), total tau (T-tau) and phosphorylated tau (P-tau) proteins in the brain and cerebrospinal fluid (CSF) of patients. However, their utility for diagnosis in routine clinical practice is still challenging because of cost, accessibility, standardization, procedural limitation, and regulatory approval. Further research is needed to establish affordable, patient-friendly, easy, quick, and robust biomarkers for early AD detection, progression, and therapeutic management. Research on blood-based preclinical diagnosis and clinical practice for AD has advanced significantly in the last decade. Emerging literature supports the importance of new molecular biomarkers and signature genes from blood to detect and predict AD in advance. This review examines the potential applications of these blood-based target biomarkers for early disease detection, co-morbid condition risk prediction, and treatment management of AD.

阿尔茨海默病（AD）是一种异质性神经退行性疾病，在早期没有标准的生物标志物来检测或确认其风险。阿尔茨海默病在全球65岁及以上人群中的患病率呈指数增长。目前的改进已经揭示了该疾病的病理生理和临床诊断测试，针对神经学变化（神经变性，淀粉样蛋白前体蛋白代谢和缠结病理），使用精确的PET/MRI成像和xMAP/SIMOA（多重同时检测/单分子阵列）来鉴定和量化患者脑和脑脊液（CSF）中的β-淀粉样蛋白（Aβ40, Aβ42），总tau （T-tau）和磷酸化tau （P-tau）蛋白。然而，由于成本、可及性、标准化、程序限制和监管批准，它们在常规临床实践中的诊断应用仍然具有挑战性。需要进一步的研究来建立负担得起的、患者友好的、简单、快速和强大的生物标志物，用于早期AD的检测、进展和治疗管理。近十年来，基于血液的阿尔茨海默病临床前诊断研究和临床实践取得了显著进展。新出现的文献支持新的分子生物标志物和血液特征基因对提前检测和预测AD的重要性。本文综述了这些基于血液的目标生物标志物在阿尔茨海默病的早期疾病检测、合并症风险预测和治疗管理中的潜在应用。

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Cognitive performance and differentiation of B-SNIP psychosis Biotypes: Algorithmic Diagnostics for Efficient Prescription of Treatments (ADEPT) - 2 B-SNIP 精神病生物类型的认知表现和区分：高效治疗处方算法诊断（ADEPT） - 2

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2024-12-24 DOI: 10.1016/j.bionps.2024.100117

Brett A. Clementz , Ishanu Chattopadhyay , S. Kristian Hill , Jennifer E. McDowell , Sarah K. Keedy , David A. Parker , Rebekah L. Trotti , Elena I. Ivleva , Matcheri S. Keshavan , Elliot S. Gershon , Godfrey D. Pearlson , Carol A. Tamminga , Robert D. Gibbons

Objective

The B-SNIP consortium validated neurobiologically defined psychosis Biotypes (BT1, BT2, BT3) using cognitive and psychophysiological measures. B-SNIP’s biomarker panel is not practical for most settings. Previously, B-SNIP developed an efficient classifier of Biotypes using only clinical assessments (called ADEPT-CLIN) with acceptable accuracy (∼.81). Adding cognitive performance may improve ADEPT’s performance.

Method

Clinical assessments from ADEPT-CLIN plus 18 cognitive measures from 1907 individuals with a B-SNIP psychosis Biotype were used to create an additional diagnostic algorithm called ADEPT-COG. Extremely randomized trees were used to create this low burden classifier.

Results

Total Biotype classification accuracy peaked at 94.6 % with 65 items. A reduced set of 18 items showed 90.5 % accuracy. Only 9–10 items achieved a one-vs-all (e.g., BT1 or not) accuracy of ∼.95, considerably better than using clinical assessments alone. The top discriminators of psychosis Biotypes were antisaccade proportion correct, BACS total, symbol coding, antisaccade correct response latency, verbal memory, digit sequencing, stop signal reaction times, stop signal proportion correct, Tower of London, and WRAT Reading. Except for antisaccade proportion correct and Tower of London, there was no overlap of the top discriminating items for B-SNIP Biotypes and DSM psychosis categories.

Conclusions

This low-burden algorithm using clinical and cognitive measures achieved high classification accuracy and can support Biotype-specific etiological and treatment investigations in clinical and research environments. It may be especially useful for clinical trials.

目标B-SNIP联盟利用认知和心理生理测量方法验证了神经生物学定义的精神病生物类型（BT1、BT2、BT3）。B-SNIP 的生物标记物面板在大多数情况下并不实用。此前，B-SNIP 仅使用临床评估（称为 ADEPT-CLIN）就开发出了一种高效的生物类型分类器，其准确性可接受（∼.81）。方法使用 ADEPT-CLIN 的临床评估结果和 1907 名 B-SNIP 精神病生物类型患者的 18 项认知测量结果，创建名为 ADEPT-COG 的附加诊断算法。结果65个项目的Biotype总分类准确率达到94.6%。减少 18 个项目后，准确率为 90.5%。只有 9-10 个项目的单项对全项（如 BT1 或非 BT1）准确率达到了 ∼.95，大大高于仅使用临床评估的准确率。对精神病生物类型的判别能力最强的是反施法正确率、BACS总分、符号编码、反施法正确反应潜伏期、言语记忆、数字排序、停止信号反应时间、停止信号正确率、伦敦塔和WRAT阅读。除了反施法正确率和伦敦塔外，B-SNIP 生物类型和 DSM 精神病类别的最高判别项目没有重叠。结论这种使用临床和认知测量的低负担算法达到了很高的分类准确性，可以支持临床和研究环境中针对生物类型的病因学和治疗调查。它可能对临床试验特别有用。

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引用次数: 0

A systematic review of neurobiological aspects of borderline personality disorder among adolescent patients 青春期边缘型人格障碍患者神经生物学方面的系统综述

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2024-12-12 DOI: 10.1016/j.bionps.2024.100114

Liliana Cruz-Ausejo , Alex Rojas-Ortega , Glauco Valdivieso-Jiménez , Anthony Copez-Lonzoy , Andrea Matayoshi , Josmel Pacheco-Mendoza , Vicente A. Benites-Zapata

Background

Borderline personality Disorder is a complex mental health condition with disturbances in emotions, self-perception, and relationships. Emerging in adolescence, it reaches its peak in early adulthood, impacting 1 %-3 % of individuals.

Methods

We documented this review in PROSPERO with the registration code CRD4202126220. Subsequently, we conducted a comprehensive search across Pubmed, PsycINFO, Medline, Embase, Web of Science and Scopus databases. A systematic synthesis focusing on the neurobiological foundations of borderline personality disorder is presented.

Results

A total of 22 studies and 1400 participants were included. Most of the studies 10/22 and 4/22 were from Australia and Germany, respectively. Genetic findings linked the short allele of 5-HTTLPR to the elevated borderline personality disorder traits and revealed neuroendocrine alterations. While imaging studies documented structural brain changes in areas such as the dorsolateral frontal gyrus and hippocampus, and reduced volumes in the anterior cingulate cortex and corpus callosum. Electrophysiological studies indicated abnormal cerebral maturation with diminished P300 amplitudes and increased alpha phase synchrony in borderline personality disorder adolescents, particularly during emotional tests.

Conclusion

We concluded that while borderline personality disorder symptoms may endure from adolescence into adulthood, existing evidence lacks consistency in neurobiological findings. Differences in the prefrontal cortex, orbitofrontal cortex, amygdala and hippocampus showed potential significance, however, electrophysiological, biochemical and genetic presented insufficient generalizable evidence for adolescents. Longitudinal studies and further investigation are needed.

边缘型人格障碍是一种复杂的心理健康状况，在情绪、自我感知和人际关系方面存在障碍。它在青春期出现，在成年早期达到顶峰，影响1 %-3 %的个体。方法我们将这篇综述发表在PROSPERO杂志上，注册码为CRD4202126220。随后，我们在Pubmed， PsycINFO, Medline, Embase， Web of Science和Scopus数据库中进行了全面的搜索。一个系统的综合集中在边缘型人格障碍的神经生物学基础提出。结果共纳入22项研究，受试者1400人。10/22和4/22的研究主要来自澳大利亚和德国。遗传研究发现，5-HTTLPR短等位基因与边缘型人格障碍特征升高有关，并揭示了神经内分泌的改变。而成像研究记录了脑结构的变化，如背外侧额回和海马体，以及前扣带皮层和胼胝体的体积减少。电生理研究表明，在边缘型人格障碍青少年中，特别是在情绪测试中，P300振幅下降和α相同步增加的异常脑成熟。结论：虽然边缘型人格障碍症状可能从青春期持续到成年，但现有证据在神经生物学研究结果中缺乏一致性。前额皮质、眶额皮质、杏仁核和海马的差异显示出潜在的显著性，但电生理、生化和遗传学方面的差异缺乏可推广的证据。需要进行纵向研究和进一步调查。

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引用次数: 0

HPA system in anxiety disorder patients treated with cognitive behavioural therapy: A review 采用认知行为疗法治疗焦虑症患者的 HPA 系统：综述

Q2 Medicine

Biomarkers in Neuropsychiatry

Pub Date : 2024-12-08 DOI: 10.1016/j.bionps.2024.100116

Jennifer Lange , Angelika Erhardt-Lehmann

Anxiety disorders (AD) have a complex etiology involving genetic, psychophysiological and environmental factors. Recent biomarker research in AD shows alterations in anatomical, biochemical and physiological pathways as well as in endocrinological processes. Perceived stress is one of the factors often reported in relation to the onset and the course of AD. Hence, the function of the hypothalamus-pituitary-adrenal (HPA) axis, the endogenous system regulating the stress response homeostasis, may serve as biomarker in disease etiology and response to treatment. Vice versa, successful treatment could have an advantageous effect on the function of the HPA system. In the present review, we summarize findings on the HPA system in relation to AD and first results on its modifiability in response to cognitive behavioral therapy (CBT), one of the most efﬁcacious psychotherapeutic treatments for AD. We specifically focus on findings of experimental studies that explored cortisol levels before, during and after exposure-based CBT. A systematic search was conducted in MEDLINE/PubMed, PsycINFO, Web of Science, and in references of retrieved studies until April 2024. The inclusion criteria were studies enclosing keywords related to the HPA axis, an anxiety disorder and CBT techniques. The results of the summarized studies suggest that cortisol levels have the potential to indicate the AD disease status and serve as possible biomarker in outcome prediction. Global dysfunction of the HPA system seems to point to higher symptom burden and less advantageous response to CBT. Furthermore, low cortisol levels elicited in relation to exposure interventions are repeatedly associated with risk for non-response. Additionally, some evidence suggests that successful CBT containing exposure sessions as well as cognitive techniques induces normalization of the HPA system by reducing acute response to fear related stimuli in parallel to normalizing basal cortisol levels. To conclude, cortisol seems to be a promising candidate to depict several aspects of AD-related disease status and CBT effects, however, additional prospective studies are needed to evaluate the mode of applications of this marker in the clinical routine.

焦虑障碍（AD）的病因复杂，涉及遗传、心理生理和环境因素。近年来的生物标志物研究表明，AD的解剖、生化和生理途径以及内分泌过程都发生了变化。感知压力是经常报道的与阿尔茨海默病发病和病程相关的因素之一。因此，调节应激反应稳态的内源性系统下丘脑-垂体-肾上腺（HPA）轴的功能可能作为疾病病因和治疗反应的生物标志物。反之，成功的治疗可以对HPA系统的功能产生有利的影响。在本综述中，我们总结了HPA系统与AD的关系，以及其对认知行为疗法（CBT）反应的可改变性的初步结果，认知行为疗法是AD最有效的心理治疗方法之一。我们特别关注实验研究的结果，这些研究探讨了基于暴露的CBT之前、期间和之后的皮质醇水平。系统检索MEDLINE/PubMed、PsycINFO、Web of Science以及检索到的研究参考文献，检索截止至2024年4月。纳入标准是包含HPA轴、焦虑障碍和CBT技术相关关键词的研究。总结的研究结果表明，皮质醇水平有可能指示AD疾病状态，并可能作为预后预测的生物标志物。HPA系统的整体功能障碍似乎指向更高的症状负担和对CBT的不利反应。此外，暴露干预引起的低皮质醇水平反复与无反应风险相关。此外，一些证据表明，成功的CBT包含暴露会话以及认知技术通过减少对恐惧相关刺激的急性反应来诱导HPA系统正常化，同时使基础皮质醇水平正常化。总之，皮质醇似乎是描述ad相关疾病状态和CBT效果的几个方面的有希望的候选者，然而，需要额外的前瞻性研究来评估该标志物在临床常规中的应用模式。

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引用次数: 0