爱丁堡大学和英国痴呆症研究所的研究人员发现，原本用于保护大脑的少突胶质细胞可能随着年龄增长而功能失调，导致产生异常过量的髓鞘，破坏神经纤维并促进认知能力下降1。这项发表在《Nature Medicine》期刊上的研究通过分析人脑组织和小鼠实验，揭示了这一过程中关键蛋白NRF2活性降低的作用1。
研究团队在Lothian Birth Cohort 1936队列中对866名参与者进行了追踪，这些参与者在70至82岁期间接受了记忆、信息处理速度和空间理解能力评估1。结果显示，认知衰退较为严重的人群体内NRF2蛋白水平明显降低1。在小鼠实验中，研究人员特异性降低少突胶质细胞中的NRF2，发现这导致过度的髓鞘形成和大神经纤维丧失1。
这一发现为治疗年龄相关的认知衰退开启了新的可能性1。已有治疗多发性硬化症的药物能够靶向NRF2通路，这些现有药物可能被重新用于对抗认知衰退1。
Scientists from the University of Edinburgh and the UK Dementia Research Institute have discovered that oligodendrocytes, brain cells meant to provide protective support, may become dysfunctional with age and fuel cognitive decline.1 The research, published in Nature Medicine on October 17, 2026, found that these cells can produce abnormally excessive myelin that damages nerve fibers and accelerates mental deterioration.1
The study examined brain tissue samples and conducted experiments in mice to identify the mechanisms underlying age-related cognitive decline.1 In the Lothian Birth Cohort 1936 study, 866 participants completed cognitive assessments between ages 70 and 82, measuring memory, information processing speed, and spatial reasoning abilities.1 Researchers observed that individuals experiencing more severe cognitive decline showed lower levels of the NRF2 protein.1 In mouse models, selectively reducing NRF2 in oligodendrocytes led to excessive myelin formation and loss of large nerve fibers.1
Existing drugs already used to treat multiple sclerosis target the NRF2 pathway and could potentially be repurposed to treat age-related cognitive decline.1
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