美国国立卫生研究院资助的一项研究揭示，人脑在中年期经历一场隐性的免疫环境重塑[1]。研究发现，从约50岁到75岁，大脑海马体中长期存在的主要免疫细胞小胶质细胞逐渐减少，被具有更强炎症特性的细胞所取代[1]。这一免疫细胞的重编程过程可能有助于解释正常衰老如何导致神经退行性疾病和痴呆症的机制[1]。
由加州大学圣迭戈分校、纽约基因组中心和加州大学欧文分校的研究人员完成的这项工作采用了先进的研究方法，结合了基因活动标准测量与表观基因组3D结构映射[1]。研究人员分析了40名年龄在20至95岁之间的神经健康成人的死后海马体组织样本[1]。研究还发现衰老与血脑屏障功能衰退相关联[1]。美国国立卫生研究院国家衰老研究所主任Richard Hodes表示："这一微胶质细胞转变可能是帮助我们完成痴呆症谜题的重要线索"[1]。这项研究已发表于《科学》杂志2026年第393卷第6809期[1]。
Researchers funded by the National Institutes of Health have identified a significant transformation in the immune environment of the brain's hippocampus starting around age 50, according to a study published in Science [1]. The research reveals that long-standing immune cells called microglia gradually diminish and are replaced by cells with stronger inflammatory signals between approximately age 50 and 75 [1].
The study analyzed postmortem hippocampal tissue samples from 40 neurologically healthy adults ranging in age from 20 to 95 years old [1]. Scientists employed advanced methodologies combining gene activity measurements with three-dimensional epigenomic structure mapping to document this cellular reprogramming [1]. The findings also associated aging with declining blood-brain barrier function [1]. According to Richard Hodes, director of the National Institute on Aging, "This microglial shift may be an important clue to help us complete the dementia puzzle" [1].
The research was conducted by investigators from the University of California, San Diego, the New York Genome Center, and the University of California, Irvine, and published in volume 393, issue 6809 of Science [1]. These findings may help explain how normal aging can lead to neurodegenerative diseases and dementia [1].