华盛顿大学圣路易斯医学院的研究团队发现了一种无需清除有害Tau蛋白就能减轻阿尔茨海默病脑损伤的治疗策略。1研究人员通过使用抗体阻断CXCR3蛋白来阻止T细胞进入大脑，在经过数月治疗后，患病小鼠脑内的T细胞数量下降约50%。1与未经治疗的小鼠相比，接受该抗体治疗的小鼠保留了约40%更多的记忆相关脑组织，并显示出记忆功能的改善。1值得注意的是，这些改善效果在Tau蛋白积聚量保持不变的情况下实现。1
研究团队指出，抗体在血脑屏障边界处起作用但不进入脑组织本身，这表明治疗效果可能通过脑外免疫调节机制实现。1研究者David M. Holtzman表示："在包括阿尔茨海默病在内的Tauopathies中，目前还没有真正降低神经变性的治疗方法。"1这项研究成果于9月28日发表在《神经元》期刊上。1
Researchers at Washington University School of Medicine in St. Louis have identified a therapeutic approach that protects brain tissue in Alzheimer's disease models by blocking the CXCR3 protein, which facilitates T cell entry into the brain 1. The strategy preserves approximately 40% more memory-related brain tissue in treated mice compared to untreated controls, despite tau protein accumulation remaining unchanged 1. The findings, published on September 28 in Neuron, demonstrate that memory improvements can occur through mechanisms independent of tau clearance 1.
The research employed antibodies to inhibit CXCR3, resulting in a roughly 50% reduction in brain T cells following months of treatment 1. Notably, the antibodies function at the blood-brain barrier boundary without entering brain tissue itself, suggesting that therapeutic benefits arise from peripheral immune modulation rather than direct central nervous system intervention 1. According to David M. Holtzman, one of the researchers: "In tauopathies, including Alzheimer's disease, there are currently no treatments that truly reduce neurodegeneration" 1.
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