据11月6日的《科学》杂志报道说，脑或者脊柱（即中枢神经系统）中的受到损伤或被切断的神经与身体其它部位的神经不同，它们不会自我修复。有关这一问题的2则新的研究探索了这一使得中枢神经系统的神经无法再生的分子学机制。这可能会为人们提出可最终帮助那些因为中枢神经系统创伤而出现严重残障和瘫痪者的神经修复途径。
在小鼠的实验中，Kevin Kyungsuk Park及其同僚展示，在去除mTOR 生长通路中的2个蛋白抑制物后，发生损伤的视神经中的神经元会在数周内重新长出来。中枢神经系统中神经元的再生还受到包裹每个神经元的髓鞘中的蛋白的抑制。这些蛋白与NgR受体相互作用从而阻断修复过程。现在，Jaswinder Atwal及其同僚发现，PirB小鼠蛋白是髓鞘蛋白阻止神经再生的另外一种受体。Woo-Yang Kim 及 William Snider在一则相关的Perspective中就这些研究将如何推动人类脊髓的治疗进行了讨论。（生物谷Bioon.com）
生物谷推荐原始出处：
Science 7 November 2008: Vol. 322. no. 5903, DOI: 10.1126/science.1161566
Promoting Axon Regeneration in the Adult CNS by Modulation of the PTEN/mTOR Pathway
Kevin Kyungsuk Park,Kai Liu,Yang Hu,Patrice D. Smith,Chen Wang, Bin Cai, Bengang Xu, Lauren Connolly, Ioannis Kramvis, Mustafa Sahin, Zhigang He
The failure of axons to regenerate is a major obstacle for functional recovery after central nervous system (CNS) injury. Removing extracellular inhibitory molecules results in limited axon regeneration in vivo. To test for the role of intrinsic impediments to axon regrowth, we analyzed cell growth control genes using a virus-assisted in vivo conditional knockout approach. Deletion of PTEN (phosphatase and tensin homolog), a negative regulator of the mammalian target of rapamycin (mTOR) pathway, in adult retinal ganglion cells (RGCs) promotes robust axon regeneration after optic nerve injury. In wild-type adult mice, the mTOR activity was suppressed and new protein synthesis was impaired in axotomized RGCs, which may contribute to the regeneration failure. Reactivating this pathway by conditional knockout of tuberous sclerosis complex 1, another negative regulator of the mTOR pathway, also leads to axon regeneration. Thus, our results suggest the manipulation of intrinsic growth control pathways as a therapeutic approach to promote axon regeneration after CNS injury.
F. M. Kirby Neurobiology Center, Children's Hospital, and Department of Neurology, Harvard Medical School, 300 Longwood Avenue, Boston, MA 02115, USA.
