KFO 256: Mechanisms of Disturbed Emotion Processing in Borderline Personality Disorder

海德堡大学(Heidelberg University)的临床研究单位(CRU)256于2012年实施，以研究边缘型人格障碍(BPD)情绪失调的神经行为基础。BPD的特点是严重的功能障碍、高自杀风险、广泛使用治疗、对他人造成伤害以及对社会的高昂成本。目前的理论认为情绪加工和社会互动功能障碍是BPD的核心机制。这通常会导致典型的行为模式，如非自杀性自残、高风险行为和冲动攻击。对BPD的心理和神经机制的研究指出，信息处理障碍、额叶边缘回路受损和获得性适应不良行为之间存在相互作用。CRU 256汇集了七个工作组的能力，每个工作组在BPD研究方面享有很高的国际声誉和/或在神经心理学、神经成像和翻译神经科学方面拥有出色的方法学专业知识。CRU的总体目标是描述BPD中功能失调的情绪处理和社会互动的子成分，并开发基于机制的个性化治疗。在CRU的第一个资助期，我们成功地理清了这些组成部分的复杂性，并在实验层面上对它们进行了研究。我们发现健康对照组和BPD患者在社会期望、信号检测、情绪激活和调节、疼痛处理和互动行为等不同领域存在显著差异。现在，我们可以利用第一个资助期的发现来设计针对BPD情绪失调和社交互动的特定机制的干预措施。特别是在个别项目(IP)1、2和5中，新的心理治疗方法将在随机对照试验中进行测试。IP8将测试第一个资助期确定的机制的药理学调节。动物模型(IP7)旨在通过病毒介导的基因转移来改变与早期社会排斥体验相关的中枢神经递质系统。此外，我们将继续对BPD的干扰机制进行研究，包括调查威胁敏感性增强、快乐面孔知觉强度降低及其与适应不良社会功能的关系(IP1、IP8)、基础互惠神经改变(IP3)、分离的神经机制(IP4)以及在自我伤害行为背景下看到血液的作用(IP6)。两个相关的项目(AP1和AP2)将由其他来源资助，专注于社会信息处理和内源性大麻素系统。该CRU的资助为海德堡大学正在进行的BPD研究平台提供了基础，该平台将对国际上关于边缘型人格障碍、社交互动和情绪调节的研究领域具有至关重要的作用。

The Clinical Research Unit (CRU) 256 at Heidelberg University was implemented in 2012 to study the neuro-behavioral underpinnings of emotion dysregulation in borderline personality disorder (BPD). BPD is characterized by severe functional impairments, a high risk of suicide, extensive use of treatment, harm to others, and high costs to society. Current theories view dysfunctions in emotion processing and social interaction as core mechanisms of BPD. This often leads to prototypical behavioral patterns such as non-suicidal self-injury, high-risk behavior, and impulsive aggression. Research on psychological and neural mechanisms of BPD points towards an interplay between dysfunctional information processing, impairments of fronto-limbic circuits, and learned maladaptive behaviors.The CRU 256 brings together the competences of seven workgroups, each with a strong international reputation in BPD research and/or excellent methodological expertise in neuropsychology, neuroimaging, and translational neuroscience. The overall aims of the CRU are to characterize subcomponents of dysfunctional emotion processing and social interaction in BPD and to develop mechanism based individualized treatments. During the first funding period of the CRU, we were successful in disentangling the complexity of these components and in studying them at an experimental level. We found significant group differences between healthy controls and BPD patients in distinct domains such as social expectations, signal detection, emotion activation and regulation, pain processing, and interactive behaviors.We can now use the findings of the first funding period to design interventions that target BPDspecific mechanisms of emotion dysregulation and social interaction. In the individual projects (IP) 1, 2, and 5 in particular, new psychological treatment approaches will be tested within randomized controlled trials. IP8 will test the pharmacological modulation of mechanisms identified in the first funding period. The animal model (IP7) aims to modify central neurotransmitter systems related to the early experience of social rejection by viral mediated gene transfer. In addition, we will continue the studies on disturbed mechanisms in BPD, including investigating enhanced threat sensitivity, reduced intensity in the perception of happy faces and its relation to maladaptive social functioning (IP1, IP8), basal neural alterations of reciprocity (IP3), neural mechanisms of dissociation (IP4), and the role of seeing blood in the context of self-injurious behavior (IP6). Two associated projects (AP1 and AP2), which will be funded by other sources, focus on social information processing and the endocannabinoid system.The funding of this CRU provides the basis for an ongoing BPD research platform at Heidelberg University that will be of critical importance to the international field of research on borderline personality disorder, social interaction, and emotion regulation.