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进展性多发性硬化症早期神经退行性变途径的鉴定

Identification of early neurodegenerative pathways in progressive multiple sclerosis.

作者信息

Kaufmann Max, Schaupp Anna-Lena, Sun Rosa, Coscia Fabian, Dendrou Calliope A, Cortes Adrian, Kaur Gurman, Evans Hayley G, Mollbrink Annelie, Navarro José Fernández, Sonner Jana K, Mayer Christina, DeLuca Gabriele C, Lundeberg Joakim, Matthews Paul M, Attfield Kathrine E, Friese Manuel A, Mann Matthias, Fugger Lars

机构信息

Institut für Neuroimmunologie und Multiple Sklerose, Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany.

Oxford Centre for Neuroinflammation, Nuffield Department of Clinical Neurosciences, John Radcliffe Hospital, University of Oxford, Oxford, UK.

出版信息

Nat Neurosci. 2022 Jul;25(7):944-955. doi: 10.1038/s41593-022-01097-3. Epub 2022 Jun 20.

Abstract

Progressive multiple sclerosis (MS) is characterized by unrelenting neurodegeneration, which causes cumulative disability and is refractory to current treatments. Drug development to prevent disease progression is an urgent clinical need yet is constrained by an incomplete understanding of its complex pathogenesis. Using spatial transcriptomics and proteomics on fresh-frozen human MS brain tissue, we identified multicellular mechanisms of progressive MS pathogenesis and traced their origin in relation to spatially distributed stages of neurodegeneration. By resolving ligand-receptor interactions in local microenvironments, we discovered defunct trophic and anti-inflammatory intercellular communications within areas of early neuronal decline. Proteins associated with neuronal damage in patient samples showed mechanistic concordance with published in vivo knockdown and central nervous system (CNS) disease models, supporting their causal role and value as potential therapeutic targets in progressive MS. Our findings provide a new framework for drug development strategies, rooted in an understanding of the complex cellular and signaling dynamics in human diseased tissue that facilitate this debilitating disease.

摘要

进展性多发性硬化症(MS)的特征是持续的神经退行性变,这会导致累积性残疾,并且对当前治疗具有抗性。开发预防疾病进展的药物是一项紧迫的临床需求,但由于对其复杂发病机制的理解不完整而受到限制。通过对新鲜冷冻的人类MS脑组织进行空间转录组学和蛋白质组学研究,我们确定了进展性MS发病机制的多细胞机制,并追踪了它们与神经退行性变的空间分布阶段相关的起源。通过解析局部微环境中的配体-受体相互作用,我们发现早期神经元衰退区域内存在失效的营养和抗炎细胞间通讯。患者样本中与神经元损伤相关的蛋白质在机制上与已发表的体内基因敲除和中枢神经系统(CNS)疾病模型一致,支持了它们在进展性MS中的因果作用和作为潜在治疗靶点的价值。我们的发现为药物开发策略提供了一个新框架,该框架基于对促进这种使人衰弱疾病的人类患病组织中复杂细胞和信号动态的理解。

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