Centre for Brain Repair, University of Cambridge, Forvie Site, Robinson Way, Cambridge CB2 0PY, UK.
Exp Eye Res. 2011 Aug;93(2):196-203. doi: 10.1016/j.exer.2010.05.016. Epub 2010 Jun 1.
Glaucoma is a progressive optic neuropathy and a major cause of visual impairment worldwide. Neuroprotective therapies for glaucoma aim to ameliorate retinal ganglion cell degeneration through direct or indirect action on these neurons. Neurotrophic factor (NTF) delivery is a key target for the development of potential neuroprotective glaucoma treatments. This article will critically summarize the evidence that NTF deprivation and/or dysfunction plays a role in the pathogenesis of glaucoma. Experimental support for the neuroprotective potential of NTF supplementation in animal models of glaucoma will be reviewed, in particular for brain-derived neurotrophic factor, ciliary neurotrophic factor, and glial cell line-derived neurotrophic factor. Finally, the challenges of clinical translation will be considered with an emphasis on the most promising NTF delivery strategies including slow-release drug delivery, gene therapy, and cell transplantation.
青光眼是一种进行性视神经病变，也是全球视力损害的主要原因。青光眼的神经保护治疗旨在通过对这些神经元的直接或间接作用来改善视网膜神经节细胞的变性。神经营养因子（NTF）的传递是开发潜在神经保护青光眼治疗方法的一个关键目标。本文将批判性地总结 NTF 剥夺和/或功能障碍在青光眼发病机制中的作用的证据。将综述 NTF 补充在青光眼动物模型中具有神经保护潜力的实验依据，特别是脑源性神经营养因子、睫状神经营养因子和胶质细胞源性神经营养因子。最后，将重点考虑临床转化的挑战，特别是最有前途的 NTF 传递策略，包括缓释药物传递、基因治疗和细胞移植。
