就像鮮花需要水的滋養(yǎng),，神經(jīng)細胞也需要某種分子的“呵護”,。英國研究人員說，他們新發(fā)現(xiàn)一種分子,，是神經(jīng)細胞的“護花者”,。
英國巴巴拉漢姆研究所的科研人員在網(wǎng)絡學術期刊《公共科學圖書館·生物卷》上報告說，一種名為Nmnat2的分子對神經(jīng)細胞具有明顯的保護作用,。這種分子通常沿著神經(jīng)元之間的突觸被輸送到各個神經(jīng)細胞。如果缺少它,，即使是健康未受傷的神經(jīng)細胞也會迅速退化,。然而，受傷的神經(jīng)細胞如果能得到這種分子的“悉心治療”,，其退化速度會明顯延緩,。
科爾曼說，如果能研發(fā)出藥物來調(diào)節(jié)這種分子在神經(jīng)細胞間的傳遞途徑,，將有助于治療早老性癡呆癥等神經(jīng)系統(tǒng)疾病,。（生物谷Bioon.com）
生物谷推薦原始出處：
PLoS Biol 8(1): e1000300. doi:10.1371/journal.pbio.1000300
Endogenous Nmnat2 Is an Essential Survival Factor for Maintenance of Healthy Axons
Jonathan Gilley, Michael P. Coleman*
The Babraham Institute, Babraham Research Campus, Cambridge, United Kingdom
The molecular triggers for axon degeneration remain unknown. We identify endogenous Nmnat2 as a labile axon survival factor whose constant replenishment by anterograde axonal transport is a limiting factor for axon survival. Specific depletion of Nmnat2 is sufficient to induce Wallerian-like degeneration of uninjured axons which endogenous Nmnat1 and Nmnat3 cannot prevent. Nmnat2 is by far the most labile Nmnat isoform and is depleted in distal stumps of injured neurites before Wallerian degeneration begins. Nmnat2 turnover is equally rapid in injured WldS neurites, despite delayed neurite degeneration, showing it is not a consequence of degeneration and also that WldS does not stabilize Nmnat2. Depletion of Nmnat2 below a threshold level is necessary for axon degeneration since exogenous Nmnat2 can protect injured neurites when expressed at high enough levels to overcome its short half-life. Furthermore, proteasome inhibition slows both Nmnat2 turnover and neurite degeneration. We conclude that endogenous Nmnat2 prevents spontaneous degeneration of healthy axons and propose that, when present, the more long-lived, functionally related WldS protein substitutes for Nmnat2 loss after axon injury. Endogenous Nmnat2 represents an exciting new therapeutic target for axonal disorders.
