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首页> 外文期刊>Experimental Neurology >Intrinsic axonal degeneration pathways are critical for glaucomatous damage
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Intrinsic axonal degeneration pathways are critical for glaucomatous damage

机译：内源性轴突变性途径对于青光眼损害至关重要

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摘要

Glaucoma is a neurodegenerative disease affecting 70million people worldwide. For some time, analysis of human glaucoma and animal models suggested that RGC axonal injury in the optic nerve head (where RGC axons exit the eye) is an important early event in glaucomatous neurodegeneration. During the last decade advances in molecular biology and genome manipulation have allowed this hypothesis to be tested more critically, at least in animal models. Data indicate that RGC axon degeneration precedes soma death. Preventing soma death using mouse models that are mutant for BAX, a proapoptotic gene, is not sufficient to prevent the degeneration of RGC axons. This indicates that different degeneration processes occur in different compartments of the RGC during glaucoma. Furthermore, the Wallerian degeneration slow allele (Wlds) slows or prevents RGC axon degeneration in rodent models of glaucoma. These experiments and many others, now strongly support the hypothesis that axon degeneration is a critical pathological event in glaucomatous neurodegeneration. However, the events that lead from a glaucomatous insult (e.g. elevated intraocular pressure) to axon damage in glaucoma are not well defined. For developing new therapies, it will be necessary to clearly define and order the molecular events that lead from glaucomatous insults to axon degeneration.
机译：青光眼是一种神经退行性疾病，影响全世界7千万人。一段时间以来，对人类青光眼和动物模型的分析表明，视神经头部的RGC轴突损伤（RGC轴突离开眼睛）是青光眼神经变性的重要早期事件。在过去的十年中，分子生物学和基因组操纵技术的进步使这一假说至少在动物模型中得到了更严格的检验。数据表明，RGC轴突变性先于躯体死亡。使用突变为BAX（一种促凋亡基因）的小鼠模型预防躯体死亡不足以预防RGC轴突的变性。这表明在青光眼期间，RGC的不同隔室中发生了不同的变性过程。此外，在青光眼的啮齿动物模型中，Wallerian变性慢等位基因（Wlds）减慢或阻止了RGC轴突变性。这些实验和许多其他实验现在强烈支持以下假设：轴突变性是青光眼神经变性中的关键病理事件。然而，由青光眼损伤（例如眼内压升高）导致青光眼轴突损伤的事件尚不清楚。为了开发新疗法，有必要明确定义和排序从青光眼损伤导致轴突变性的分子事件。

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