Coordination Funds

协调基金

基本信息

项目摘要

The gut-brain axis is a bidirectional communication system driven by neural, hormonal, metabolic, immunological, and microbial signals. Signaling events from the gut can modulate brain function and recent evidence suggests that a dysregulated gut-brain axis plays a pivotal role in linking gastrointestinal and neurological diseases. In this context, clinical data reveal that patients with Inflammatory Bowel Disease (IBD) are at higher risk of subsequently developing Parkinson's disease (PD). In addition, the association between Multiple Sclerosis (MS) and IBD has been suggested, apart from their common epidemiological and immunological patterns, also due to observations of increased incidence of both IBD among MS patients and MS among IBD patients. Accordingly, a bidirectional link between gastrointestinal inflammation and neurodegeneration/ neuroinflammation, in accordance with the idea of the ‘gut–brain axis’, has recently emerged. In particular, enteric dysbiosis, translocation of bacterial products as well as inflammatory cells/soluble factors derived from the inflamed intestinal mucosa across the gut epithelial- and blood-brain-barrier (BBB) have been implicated as major factors for structural and functional alterations in the CNS. While the concept of a pathophysiological gut-brain axis is increasingly recognized, in-depth characterization of inter-organ communication to identify immunological checkpoints that control this network during health and disease, is limited. The overall aim of this clinical research unit is to delineate the interactions between the intestinal and the nervous system across the gut-brain axis in the context of immune-mediated inflammatory and degenerative diseases. Cross-fertilization between the research foci immunology and neuroscience will allow us to gain unique new insights into the pathogenesis of these disorders to establish the necessary scientific foundation for the future development of novel diagnostic and therapeutic tools. Controlling the disease activity in one of the organs may reduce the risk of developing inflammation/degeneration in the other direction of the axis, potentially owing to a reduction in disease activity and modulation of the gut-brain axis. To reach this goal, we will combine our strong expertise in basic and clinical neuroimmunology, neurodegeneration, gastroenterology, and mucosal immunology. Using a strictly interdisciplinary approach, we aim for the replacement of the traditionally organ centered perception of inflammation. In the long-term perspective, we aim to obtain a comprehensive understanding of gut-brain communication for the identification of novel biomarkers, therapeutic targets, interventional strategies and predictors of treatment response to improve patient care.
肠-脑轴是由神经、激素、代谢、免疫和微生物信号驱动的双向通信系统。来自肠道的信号事件可以调节大脑功能,最近的证据表明,失调的肠-脑轴在连接胃肠道和神经系统疾病中起着关键作用。在这种情况下,临床数据显示,炎症性肠病(IBD)患者随后发生帕金森病(PD)的风险较高。此外,除了其常见的流行病学和免疫学模式外,还由于观察到MS患者中IBD和IBD患者中MS的发病率增加,提示多发性硬化症(MS)和IBD之间存在相关性。因此,最近出现了胃肠道炎症和神经变性/神经炎症之间的双向联系,与“肠-脑轴”的想法一致。特别是,肠道生态失调,细菌产物的易位以及炎症细胞/可溶性因子来源于发炎的肠粘膜穿过肠上皮和血脑屏障(BBB)已被认为是CNS结构和功能改变的主要因素。虽然病理生理学肠-脑轴的概念越来越受到认可,但对器官间通讯的深入表征以识别在健康和疾病期间控制该网络的免疫检查点却很有限。该临床研究单位的总体目标是在免疫介导的炎症和退行性疾病的背景下,描述肠道和神经系统在肠-脑轴上的相互作用。免疫学和神经科学研究领域之间的交叉将使我们能够对这些疾病的发病机制获得独特的新见解,为未来开发新的诊断和治疗工具建立必要的科学基础。控制一个器官中的疾病活动可以降低在轴的另一个方向上发生炎症/变性的风险,这可能是由于疾病活动的减少和肠-脑轴的调节。为了实现这一目标,我们将联合收割机结合我们在基础和临床神经免疫学、神经变性、胃肠病学和粘膜免疫学方面的强大专业知识。使用严格的跨学科方法,我们的目标是取代传统的以器官为中心的炎症感知。从长远来看,我们的目标是全面了解肠-脑通信,以确定新的生物标志物,治疗靶点,干预策略和治疗反应的预测因子,以改善患者护理。

项目成果

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Professorin Dr. Beate Winner其他文献

Professorin Dr. Beate Winner的其他文献

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{{ truncateString('Professorin Dr. Beate Winner', 18)}}的其他基金

Deciphering the physiological role of Spastin for the regulation of Store Operated Calcium Entry and its pathological consequences in iPSC Derived SPG4 Neurons
破译 Spastin 在 iPSC 衍生 SPG4 神经元中调节钙库操作钙进入的生理作用及其病理后果
  • 批准号:
    439144457
  • 财政年份:
    2020
  • 资助金额:
    --
  • 项目类别:
    Research Grants

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