Institute of Biochemistry and Cell Biology, Institute of Biochemistry and Cell Biology, National Research Council (IBBC/CNR), Monterotondo, 00015 Rome, Italy.
Plaisant S.R.L., 00128 Rome, Italy.
Int J Mol Sci. 2023 Feb 2;24(3):2911. doi: 10.3390/ijms24032911.
Traumatic brain injury (TBI) represents one of the most common worldwide causes of death and disability. Clinical and animal model studies have evidenced that TBI is characterized by the loss of both gray and white matter, resulting in brain atrophy and in a decrease in neurological function. Nowadays, no effective treatments to counteract TBI-induced neurological damage are available. Due to its complex and multifactorial pathophysiology (neuro-inflammation, cytotoxicity and astroglial scar formation), cell regeneration and survival in injured brain areas are strongly hampered. Recently, it has been proposed that adult neurogenesis may represent a new approach to counteract the post-traumatic neurodegeneration. In our laboratory, we have recently shown that physical exercise induces the long-lasting enhancement of subventricular (SVZ) adult neurogenesis in a p21 (negative regulator of neural progenitor proliferation)-null mice model, with a concomitant improvement of olfactory behavioral paradigms that are strictly dependent on SVZ neurogenesis. On the basis of this evidence, we have investigated the effect of running on SVZ neurogenesis and neurorepair processes in p21 knock-out mice that were subject to TBI at the end of a 12-day session of running. Our data indicate that runner p21 ko mice show an improvement in numerous post-trauma neuro-regenerative processes, including the following: (i) an increase in neuroblasts in the SVZ; (ii) an increase in the migration stream of new neurons from the SVZ to the damaged cortical region; (iii) an enhancement of new differentiating neurons in the peri-lesioned area; (iv) an improvement in functional recovery at various times following TBI. All together, these results suggest that a running-dependent increase in subventricular neural stem cells could represent a promising tool to improve the endogenous neuro-regenerative responses following brain trauma.
创伤性脑损伤(TBI)是全球最常见的死亡和残疾原因之一。临床和动物模型研究表明,TBI 的特征是灰质和白质的丧失,导致脑萎缩和神经功能下降。目前,尚无有效的治疗方法来对抗 TBI 引起的神经损伤。由于其复杂的多因素病理生理学(神经炎症、细胞毒性和星形胶质瘢痕形成),受损大脑区域的细胞再生和存活受到严重阻碍。最近,有人提出成年神经发生可能是对抗创伤后神经退行性变的新方法。在我们的实验室中,我们最近表明,运动可在 p21(神经祖细胞增殖的负调节剂)缺失小鼠模型中持久增强侧脑室下区(SVZ)的成年神经发生,同时改善严格依赖 SVZ 神经发生的嗅觉行为范式。基于这一证据,我们研究了在 12 天跑步期结束后遭受 TBI 的 p21 敲除小鼠中跑步对 SVZ 神经发生和神经修复过程的影响。我们的数据表明,跑步的 p21 敲除小鼠在许多创伤后神经再生过程中表现出改善,包括以下几个方面:(i)SVZ 中的神经前体细胞增加;(ii)从 SVZ 到受损皮质区域的新神经元迁移流增加;(iii)损伤周围区域的新分化神经元增强;(iv)TBI 后不同时间的功能恢复改善。总之,这些结果表明,SVZ 神经干细胞的跑步依赖性增加可能是改善脑创伤后内源性神经再生反应的有前途的工具。