摘要
青光眼是一群多因性的神經退化之疾病，主要以視神經和視網膜神經節細胞緩慢而持續性的損害為特徵，同時在視野上亦表現出和此損害相當的視野缺損。傳統上眼壓升高被認為是青光眼最重要的危險因子之一，也是導致青光眼的主因；然而在臨床上部分青光眼的患者並不能經由降低眼壓而對其視神經與視野達到有效的保護，因此必須尋求其他的治療方式。目前研究青光眼治療的趨勢著重在透過分子生物學的管道保護尚未損壞的神經免於受損，或挽救已經受損的神經使其復原。在本文中我們將討論三種主要的青光眼神經退化之機轉（機械性傷害理論、血流障礙假說以及自體免疫假說），並探討青光眼神經保護療法的標的；同時我們也將檢視目前已知的神經保護藥物，並說明這些藥物應用在青光眼治療上的可行性。最後文中將提出最近尚在試驗階段的分子生物學領域之青光眼神經保護療法之進展。目前已有許多被證實能有效保護神經的途徑可應用於青光眼，然而如何使這些知識成為臨床上具體可行治療方式仍是急需克服的最大挑戰。
並列摘要
Glaucoma is a group of multifactorial, neurodegenerative diseases characterized by slow progressive damage to the optic nerve and retinal ganglion cells (RGCs). Visual field defects corresponding to the damage can be identified. Traditionally, elevated intraocular pressure (IOP) is regarded as the most important risk factor and the possible primary insult in glaucoma. However, lowering the IOP is unable in some cases to control progressive optic nerve damage and prevent further vision loss satisfactorily. Hence, additional treatment strategies are needed. Currently, the focus of research in glaucoma treatment is shifting toward neuroprotection, which may be defined as the protection of undamaged RGCs and the rescue of injured RGCs by therapeutic agents or through molecular and cell-based approaches. In this article, three mechanisms of glaucoma neurodegeneration (the mechanical theory, the vascular hypothesis and autoimmunity) will be discussed, and possible targets for glaucoma neuroprotection will be identified. In addition, we will evaluate currently advocated neuroprotective drugs and discuss their potential in the management of glaucoma. Finally, we will also review novel molecular and cell-based approaches as well as a variety of experimental strategies for neuroprotection against glaucoma. There is, indeed, a wealth of knowledge may help to identify effective glaucoma neuroprotection. The challenge now is how to assess the way forward to make this approach become useful.
延伸閱讀
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- 林君玉（2002）。青光眼的治療經驗。中醫藥研究論叢，5(1)，14-16。https://doi.org/10.6516/TJTCM.200203_5(1).0003
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