由纽约基因组中心、哥伦比亚大学、加州大学圣地亚哥分校和加州大学欧文分校组成的研究团队发现，人脑在50至75岁期间经历了基因组调控的广泛变化1。该研究成果发表在《科学》杂志上，是美国国立卫生研究院4D核体项目十年倡议的六篇论文之一1。
研究表明，在这一关键时期，小胶质细胞大幅下降，并被具有更强炎症特征的血源性免疫细胞所替代1。同时，维持血脑屏障的细胞群体也实质性下降1。多种脑细胞类型中观察到的三维基因组结构广泛侵蚀进一步加剧了这些变化1。
研究团队负责人Bing Ren博士表示："当这些细胞未能履行其管家职责时，有毒物质积累可能引发炎症过程，可能导致神经退行性疾病"1。这项发现或可解释为何衰老是阿尔茨海默病等神经退行性疾病的最强风险因素1。
Researchers have identified significant genomic regulatory changes that occur in the human brain during midlife, with the most dramatic transformation happening between ages 50 and 75.1 The study, published in Science on September 15, 2026, reveals that microglia—immune cells crucial for brain maintenance—substantially decline during this period and are replaced by blood-derived immune cells that exhibit stronger inflammatory characteristics.1 This replacement is accompanied by widespread deterioration of three-dimensional genome structure across multiple brain cell types, a finding that may explain why aging is the strongest risk factor for neurodegenerative diseases such as Alzheimer's disease.1
The research, conducted by teams from the New York Genome Center, Columbia University, UC San Diego, and UC Irvine, also documents a substantial decrease in blood-brain barrier-maintaining cells during this critical window.1 According to Dr. Bing Ren, "When these cells fail to perform their housekeeping duties, toxic substances can accumulate and trigger inflammatory processes that may lead to neurodegeneration."1 This study is one of six Science papers resulting from a decade-long initiative by the U.S. National Institutes of Health's 4D Nucleome (4DN) project, underscoring the collaborative effort to understand fundamental aspects of brain aging at the genomic level.1
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