據(jù)11月6日的《科學(xué)》雜志報道說,，腦或者脊柱（即中樞神經(jīng)系統(tǒng)）中的受到損傷或被切斷的神經(jīng)與身體其它部位的神經(jīng)不同,，它們不會自我修復(fù)。有關(guān)這一問題的2則新的研究探索了這一使得中樞神經(jīng)系統(tǒng)的神經(jīng)無法再生的分子學(xué)機制,。這可能會為人們提出可最終幫助那些因為中樞神經(jīng)系統(tǒng)創(chuàng)傷而出現(xiàn)嚴重殘障和癱瘓者的神經(jīng)修復(fù)途徑,。
在小鼠的實驗中,，Kevin Kyungsuk Park及其同僚展示,，在去除mTOR 生長通路中的2個蛋白抑制物后,，發(fā)生損傷的視神經(jīng)中的神經(jīng)元會在數(shù)周內(nèi)重新長出來。中樞神經(jīng)系統(tǒng)中神經(jīng)元的再生還受到包裹每個神經(jīng)元的髓鞘中的蛋白的抑制,。這些蛋白與NgR受體相互作用從而阻斷修復(fù)過程。現(xiàn)在,，Jaswinder Atwal及其同僚發(fā)現(xiàn),，PirB小鼠蛋白是髓鞘蛋白阻止神經(jīng)再生的另外一種受體。Woo-Yang Kim 及 William Snider在一則相關(guān)的Perspective中就這些研究將如何推動人類脊髓的治療進行了討論,。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
