Neuroinflammation and Aggression

神经炎症和攻击行为

• 批准号: 9315925
• 负责人: EMIL Frank COCCARO
• 金额: $ 60.46万
• 依托单位: UNIVERSITY OF CHICAGO
• 依托单位国家: 美国
• 财政年份: 2015
• 资助国家: 美国
• 起止时间: 2015-08-13 至 2019-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/9315925
• 关键词: Adult; Aggressive behavior; Amygdaloid structure; Anger; Animal Model; Animals; Behavior; Behavioral; Biological; Brain; Brain region; C-reactive protein; Case-Control Studies; Cerebrospinal Fluid; Data; Dimensions; Disease remission; Emotional; Endotoxins; Face; Functional Magnetic Resonance Imaging; Gene Expression; Habits; Health; Hostility; Human; IL2 gene; IL8 gene; Impulsivity; Individual; Inflammation; Inflammation Mediators; Inflammatory; Inflammatory Response; Injury; Interleukin-1 beta; Interleukin-10; Interleukin-2; Interleukin-6; LIF gene; Lead; Measures; Mediator of activation protein; Mental Depression; N-Methyl-D-Aspartate Receptors; Nature; Neuraxis; Neuromodulator; Neurons; Neurotransmitters; Obesity; Pathway interactions; Peripheral; Pilot Projects; Plasma; Play; Process; Proteins; Psychometrics; Psychosocial Stress; Recurrence; Role; Serotonin; Serotonin Agents; Serum; Serum Markers; Signal Transduction; Site; Societies; Structure; System; TNF gene; Testing; Tryptophan; Tryptophan Metabolism Pathway; Work; base; blood oxygenation level dependent response; cytokine; follow-up; human subject; inflammatory marker; information processing; insight; neural circuit; neurochemistry; neuroinflammation; pre-clinical; prospective; public health relevance; response; social; social neuroscience

 DESCRIPTION (provided by applicant): In this application, we propose to build on previous work regarding the role of neuroinflammation in aggression and in social-emotional information processing. Both preclinical animal studies and recent human studies from our lab, and other labs, support the hypothesis that inflammatory processes are an important modulator that facilitates aggressive behavior. Work in human subjects have all been from the study of peripheral, as opposed to central, inflammatory marker/mediators and have been limited to only one or two markers (e.g., C-Reactive Protein and IL-6). In this study, we propose to test the hypothesis that: (a) various inflammatory marker/mediators in the central nervous system (i.e., measured in cerebrospinal fluid) are dimensionally related to aggressive behavior (i.e., if they mirror, and/or better relate to aggression than, peripheral inflammatory measures) and, (b) that these inflammatory marker/mediators play a role in social-emotional information processing, an important component of human aggressive behavior, as expected based on experimental work in human subjects and from our own pilot data.

 描述（由申请人提供）：在本申请中，我们建议建立在以前的工作有关神经炎症的作用，在侵略和社会情绪信息处理。我们实验室和其他实验室的临床前动物研究和最近的人类研究都支持炎症过程是促进攻击行为的重要调节剂的假设。在人类受试者中的工作都来自外周（与中枢相反）炎症标志物/介质的研究，并且仅限于一种或两种标志物（例如，C-反应蛋白和IL-6）。在这项研究中，我们提出测试假设：（a）中枢神经系统中的各种炎症标志物/介质（即，在脑脊髓液中测量）在尺寸上与攻击行为相关（即，如果它们反映和/或比外周炎症测量更好地与攻击性相关），和（B）这些炎症标记物/介质在社会情绪信息处理中发挥作用，社会情绪信息处理是人类攻击性行为重要组成部分，如基于人类受试者的实验工作和我们自己的试验数据所预期的。