苏黎世大学的研究人员发现，成年脑在损伤后的自我修复能力超出了科学家的既有认知1。研究团队通过对小鼠的实时观察发现，一种名为星形胶质细胞的支持细胞能够通过将新产生的细胞核沿着细胞延伸体传输到受损区域，从而重建被破坏的星形胶质细胞网络1。该研究由苏黎世大学药理学和毒理学研究所的Marina Herwerth和Matthias Wyss共同领导，Bruno Weber为研究团队负责人，已发表于2026年《自然神经科学》第29卷第8期1。
研究人员使用双光子显微镜对活体小鼠脑部进行了数周的实时追踪，记录了脑部不同区域在修复过程中的基因激活情况1。研究发现了多个在修复期间暂时激活的基因和信号通路1。Bruno Weber表示："我们能够识别许多在修复期间暂时激活的基因和信号通路。它们可能在将来作为影响疾病后和损伤后再生过程的起点。"1这些发现为脑损伤患者的治疗提供了新的靶点方向。
此外，来自Max Planck精神病学研究所的研究也揭示了脑部修复的另一个关键机制2。研究人员发现应激激素皮质促激素释放激素（CRH）在脑损伤后会被少突胶质细胞前体激活并释放，从而调控这些细胞的成熟过程并帮助重建髓鞘2。CRH反应在损伤后几小时内可被检测到，约三天后停止2。缺少CRH受体1的小鼠在损伤后少突胶质细胞前体增殖更快，但最终成熟的少突胶质细胞反而更少2，这表明CRH系统在调节修复过程中的关键作用。
Researchers at the University of Zurich have discovered that the adult brain can repair itself more effectively than scientists had thought, revealing a previously underappreciated regenerative mechanism in response to neurological damage 1. The team identified a process by which specialized support cells called astrocytes reconstruct damaged networks by transporting newly formed cell nuclei across long distances through cellular extensions to injured brain regions 1.
The research, published in Nature Neuroscience, volume 29, issue 8 in 2026 1, was conducted in mice and employed two-photon microscopy to observe living brain tissue in real time over several weeks, tracking gene activation patterns across different brain regions 1. The study, led by Marina Herwerth and Matthias Wyss from the Institute of Pharmacology and Toxicology at the University of Zurich, with Bruno Weber as the research team leader 1, identified numerous genes and signaling pathways that become temporarily active during the repair process, which could serve as potential therapeutic targets for facilitating regeneration following disease and injury 1. According to Bruno Weber, "We were able to identify many genes and signaling pathways that are temporarily activated during repair. They may in the future serve as starting points for influencing regeneration processes after disease and injury" 1.
In parallel work, scientists at the Max Planck Institute of Psychiatry have uncovered another mechanism of neural self-repair, demonstrating that a stress hormone called corticotropin-releasing hormone (CRH) helps the brain mend itself following injury 2. When brain damage occurs, oligodendrocyte precursor cells rapidly release CRH, which regulates the maturation of these cells and aids in rebuilding myelin, the protective coating around neurons 2. This CRH response can be detected within hours of injury and typically subsides after approximately three days 2.
The findings suggest that mice lacking CRH receptor 1 show accelerated proliferation of oligodendrocyte precursor cells following injury, yet ultimately produce fewer mature oligodendrocytes 2. During normal brain development, these same mice exhibited thicker myelin around axons 2. Researchers speculate that the CRH system may play a larger role in stress-related psychiatric disorders such as depression 2.
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