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High-dose radiation with bone marrow transfer prevents neurodegeneration in an inherited glaucoma

机译:高剂量放射与骨髓移植可预防遗传性青光眼的神经变性

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Here, we show that high-dose y-irradiation accompanied with syngeneic bone marrow transfer can confer complete protection against glaucoma in a mouse model. Because bone marrow genotype was unaltered by this procedure, it was not the causative agent. The neuroprotection is robust and highly reproducible. Glaucoma-prone DBA/2J mice received a single treatment at 5-8 weeks of age and were protected from glaucomatous retinal ganglion cell degeneration out to 14 months of age (oldest assessed). By 12-14 months, retinal ganglion cell degeneration is usually very severe and essentially complete in the majority of untreated DBA/2J mice. To assess reproducibility, three groups of mice were treated at different times, and the results were essentially the same each time. Considering all experiments, the vast majority of treated mice had no detectable glaucomatous neurodegeneration. A beneficial effect of treatment including high-dose radiation is unprecedented, and we are not aware of any other neuroprotective effects this substantial. Because of the robust protective effect, this treatment offers another tool for studying mechanisms of neuroprotection.
机译:在这里,我们显示高剂量γ射线辐射伴随同基因骨髓转移可以在小鼠模型中赋予针对青光眼的完全保护。由于此操作不会改变骨髓基因型,因此它不是病原体。神经保护作用牢固且可重现。易患青光眼的DBA / 2J小鼠在5-8周龄时接受了一次治疗,并在14个月龄时免受青光眼性视网膜神经节细胞变性的影响(评估最久)。到12-14个月时,在大多数未经治疗的DBA / 2J小鼠中,视网膜神经节细胞变性通常非常严重并且基本完成。为了评估可重复性,在不同的时间对三组小鼠进行了处理,每次结果基本相同。考虑到所有实验,绝大多数经治疗的小鼠均未检测到青光眼神经变性。包括高剂量放射在内的治疗效果是前所未有的,而且我们还没有发现其他任何实质性的神经保护作用。由于强大的保护作用,这种治疗方法为研究神经保护机制提供了另一种工具。

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