就像鲜花需要水的滋养，神经细胞也需要某种分子的“呵护”。英国研究人员说，他们新发现一种分子，是神经细胞的“护花者”。
英国巴巴拉汉姆研究所的科研人员在网络学术期刊《公共科学图书馆·生物卷》上报告说，一种名为Nmnat2的分子对神经细胞具有明显的保护作用。这种分子通常沿着神经元之间的突触被输送到各个神经细胞。如果缺少它，即使是健康未受伤的神经细胞也会迅速退化。然而，受伤的神经细胞如果能得到这种分子的“悉心治疗”，其退化速度会明显延缓。
科尔曼说，如果能研发出药物来调节这种分子在神经细胞间的传递途径，将有助于治疗早老性痴呆症等神经系统疾病。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
