Lindvall Olle, Kokaia Zaal
Laboratory of Stem Cells and Restorative Neurology, Lund Stem Cell Center, University Hospital, SE-221 84 Lund, Sweden.
Cold Spring Harb Perspect Biol. 2015 Nov 2;7(11):a019034. doi: 10.1101/cshperspect.a019034.
A bulk of experimental evidence supports the idea that the stroke-damaged adult brain makes an attempt to repair itself by producing new neurons also in areas where neurogenesis does not normally occur (e.g., the striatum and cerebral cortex). Knowledge about mechanisms regulating the different steps of neurogenesis after stroke is rapidly increasing but still incomplete. The functional consequences of stroke-induced neurogenesis and the level of integration of the new neurons into existing neural circuitries are poorly understood. To have a substantial impact on the recovery after stroke, this potential mechanism for self-repair needs to be enhanced, primarily by increasing the survival and differentiation of the generated neuroblasts. Moreover, for efficient repair, optimization of neurogenesis most likely needs to be combined with promotion of other endogenous neuroregenerative responses (e.g., protection and sprouting of remaining mature neurons, transplantation of neural stem/progenitor cells [NSPC]-derived neurons and glia cells, and modulation of inflammation).
大量实验证据支持这样一种观点，即中风损伤的成人大脑会试图通过在神经发生通常不会发生的区域（如纹状体和大脑皮层）产生新的神经元来进行自我修复。关于中风后调节神经发生不同步骤的机制的知识正在迅速增加，但仍然不完整。中风诱导的神经发生的功能后果以及新神经元整合到现有神经回路中的程度仍知之甚少。为了对中风后的恢复产生实质性影响，这种自我修复的潜在机制需要得到增强，主要是通过提高所产生的神经母细胞的存活率和分化率。此外，为了实现有效的修复，神经发生的优化很可能需要与促进其他内源性神经再生反应（如保护剩余的成熟神经元并使其发芽、移植神经干细胞/祖细胞[NSPC]衍生的神经元和神经胶质细胞以及调节炎症）相结合。
