科隆大学研究团队在《Nature Aging》杂志发表最新研究，揭示了EPS8蛋白在衰老过程中如何引发神经退行性疾病[1]。研究表明，这种蛋白质随着年龄增长而不断积累，激活导致有毒蛋白聚集的应激反应，进而损害神经元功能[1]。该发现为肌萎缩侧索硬化症（ALS）和亨廷顿病等老年神经退行性疾病提供了新的药物靶点[1]。
研究人员在线虫和人类细胞模型中均验证了这一机制[1]。关键发现是降低EPS8的活性可以有效防止病理性蛋白聚集的形成，从而保护神经功能[1]。这表明EPS8及其相关信号通路的作用机制在不同生物体系中具有保守性[1]。
Researchers at the University of Cologne have uncovered a molecular mechanism by which aging triggers neurodegenerative disease, pointing to a protein called EPS8 as a critical culprit.[1] The team found that EPS8 accumulates with advancing age and activates cellular stress responses that lead to the buildup of toxic proteins, ultimately damaging neurons.[1] This discovery, published in Nature Aging in September 2025, opens new possibilities for treating age-related neurological conditions including amyotrophic lateral sclerosis (ALS) and Huntington's disease.[1]
The research was conducted by David Vilchez and colleagues at the CECAD Cluster of Excellence for Aging Research at the University of Cologne.[1] Working in both Caenorhabditis elegans roundworms and human cells, the team demonstrated that reducing EPS8 activity can prevent the harmful accumulation of proteins and protect neuronal function.[1] The EPS8 signaling pathway and its role in protein aggregation were found to be conserved across these model systems, suggesting the mechanism may be broadly relevant to human disease.[1] These findings identify EPS8 and its associated signaling pathways as potential drug targets for developing new therapies to combat age-related neurodegeneration.[1]