In the injured brain, new neurons produced from endogenous neural stem cells form chains and migrate to injured areas and contribute to the regeneration of lost neurons. However, this endogenous regenerative capacity of the brain has not yet been leveraged for the treatment of brain injury. Here, we show that in healthy brain chains of migrating new neurons maintain unexpectedly large non-adherent areas between neighboring cells, allowing for efficient migration. In instances of brain injury, neuraminidase reduces polysialic acid levels, which negatively regulates adhesion, leading to increased cell-cell adhesion and reduced migration efficiency. The administration of zanamivir, a neuraminidase inhibitor used for influenza treatment, promotes neuronal migration toward damaged regions, fosters neuronal regeneration, and facilitates functional recovery. Together, these findings shed light on a new mechanism governing efficient neuronal migration in the adult brain under physiological conditions, pinpoint the disruption of this mechanism during brain injury, and propose a promising therapeutic avenue for brain injury through drug repositioning.

中文翻译：

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神经氨酸酶抑制促进神经元的集体迁移和脑功能的恢复。


在受伤的大脑中，内源性神经干细胞产生的新神经元形成链并迁移到受伤区域，并有助于丢失神经元的再生。然而，大脑的这种内源性再生能力尚未用于治疗脑损伤。在这里，我们表明，在健康的大脑中，新神经元的迁移链在相邻细胞之间保持出乎意料的大的非粘附区域，从而实现有效的迁移。在脑损伤的情况下，神经氨酸酶会降低聚唾液酸水平，从而对粘附产生负面调节，导致细胞间粘附增加并降低迁移效率。扎那米韦（一种用于流感治疗的神经氨酸酶抑制剂）的给药可促进神经元向受损区域迁移，促进神经元再生并促进功能恢复。总之，这些发现揭示了生理条件下控制成人大脑有效神经元迁移的新机制，查明了脑损伤期间该机制的破坏，并提出了通过药物重新定位治疗脑损伤的有前景的治疗途径。