华盛顿大学医学院的研究团队发现，阿尔茨海默病相关的脑损伤可能由脑外免疫通路驱动。1 研究表明，T细胞在淋巴结中接收激活信号后进入大脑，引发神经退行性变化，而非在脑内直接激活。1 该发现已于2026年9月3日发表在《自然神经科学》期刊上。1
研究团队在小鼠模型中通过消除淋巴结中的树突状细胞来阻断这一信号通路。1 结果显示，脑内CD8 T细胞数量大幅下降，脑损伤消失，小鼠的认知能力得以保护。1 值得注意的是，这种保护作用出现在Tau缠结数量不变的情况下，提示即使Tau缠结存在，也可能通过阻断免疫通路来减缓认知衰退。1
由David M. Holtzman博士领导的研究团队指出，该免疫通路在脑外运作，可能提供更易触及的治疗靶点，无需药物穿过血脑屏障。1 这一发现为开发阿尔茨海默病和其他Tau相关神经退行性疾病的新型治疗策略提供了潜在方向。1
Researchers at Washington University School of Medicine have discovered that brain damage associated with Alzheimer's disease may be driven by an immune pathway operating outside the brain itself.1 The study reveals that T cells become activated in lymph nodes and subsequently enter the brain, triggering neurodegeneration, rather than being activated within brain tissue.1 When researchers blocked this signaling pathway in mouse models, they observed a significant reduction in neurodegeneration and protection of cognitive function.1 The findings were published in Nature Neuroscience on September 3, 2026.1
The research team, led by Dr. David M. Holtzman of the Department of Neurology at Washington University School of Medicine, found that removing dendritic cells from lymph nodes resulted in a dramatic decrease in CD8 T cells in the brain and elimination of brain injury.1 Cognitive abilities were preserved in mice, even though tau tangles—a hallmark of Alzheimer's pathology—remained unchanged.1 This finding suggests that cognitive decline may potentially be slowed even when tau tangles are present.1 Because this immune pathway operates outside the brain, it may offer a more readily accessible therapeutic target that does not require medications to cross the blood-brain barrier.1
评论
还没有评论，欢迎留下第一条。