Weber A J, Harman C D, Viswanathan S
Department of Physiology, Michigan State University, East Lansing, MI 48824, USA.
J Physiol. 2008 Sep 15;586(18):4393-400. doi: 10.1113/jphysiol.2008.156729. Epub 2008 Jun 19.
Glaucoma is an optic neuropathy that originates with pressure-induced damage to the optic nerve. This results in the retrograde degeneration of ganglion cells in the retina, and a progressive loss of vision. Over the past several years, a number of studies have described the structural and functional changes that characterize ganglion cell degeneration in the glaucomatous eye, and following optic nerve injury. In addition, a variety of different strategies for providing neuroprotection to the injured retina have been proposed. Many of these are based on the use of brain-derived neurotrophic factor (BDNF), a particularly potent neuroprotectant in the mammalian eye and the basis of our research in this area. Of particular importance is the fact that BDNF not only promotes ganglion cell survival following damage to the optic nerve, but also helps to preserve the structural integrity of the surviving neurons, which in turn results in enhanced visual function. The studies presented here describe these attributes, and serve as the foundation for ongoing work that suggests a need to think beyond the eye in the development of future treatment strategies.
青光眼是一种视神经病变,源于眼压对视神经造成的损伤。这会导致视网膜中神经节细胞逆行性变性,并逐渐丧失视力。在过去几年中,多项研究描述了青光眼性眼及视神经损伤后神经节细胞变性的结构和功能变化。此外,还提出了多种为受损视网膜提供神经保护的不同策略。其中许多策略基于使用脑源性神经营养因子(BDNF),它在哺乳动物眼中是一种特别有效的神经保护剂,也是我们在该领域研究的基础。特别重要的是,BDNF不仅能促进视神经损伤后神经节细胞的存活,还有助于维持存活神经元的结构完整性,进而增强视觉功能。这里介绍的研究描述了这些特性,并为正在进行的工作奠定了基础,这些工作表明在未来治疗策略的开发中需要跳出眼睛的局限去思考。