GAMMA SYNUCLEIN AGGREGATES AND GLAUCOMA

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 青光眼是一种神经退行性疾病，杀死视网膜神经节细胞，是世界范围内第二大致盲原因。我们最近在多种青光眼动物模型中的数据表明，这种疾病的特征在于γ突触核蛋白（Sncg）的病理形式，类似于帕金森病中α突触核蛋白的病理形式。为了揭示这些Sncg形式的性质，我们提出了电子和免疫电子显微镜分析的视神经乳头在小鼠模型青光眼，DBA/2 J小鼠，和轴突和终端的转基因青蛙过度表达标记的Sncg在视网膜神经节细胞。通过证明青光眼和帕金森病中常见的细胞病理学，目前的研究将对这两种同样常见的神经退行性疾病的当前研究和未来治疗产生重大影响。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Glaucoma is a neurodegenerative disorder that kills retinal ganglion cells and is the second leading cause of blindness worldwide. Our recent data in multiple animal models of glaucoma suggest that this disease is characterized by pathological forms of gamma synuclein (Sncg) that resemble those seen for alpha synuclein in Parkinson's disease. In order to uncover the nature of these Sncg forms, we propose electron and immunoelectron microscopy analyses of the optic nerve head in a mouse model of glaucoma, the DBA/2J mouse, and of axons and terminals of transgenic frogs that overexpress tagged-Sncg in retinal ganglion cells. By demonstrating common cellular pathology in glaucoma and Parkinson's disease, the current studies stand to have a large impact on the current study and future treatment of these two equally common neurodegenerative disorders.