GAMMA SYNUCLEIN AGGREGATES AND GLAUCOMA

伽玛突触核蛋白聚集体和青光眼

• 批准号: 8169646
• 负责人: NICHOLAS R MARSH-ARMSTRONG
• 金额: $ 2.39万
• 依托单位: UNIVERSITY OF CALIFORNIA, SAN DIEGO
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169646
• 关键词: Animal Model; Blindness; Computer Retrieval of Information on Scientific Projects Database; Data; Disease; Electrons; Funding; Future; Gamma synuclein; Glaucoma; Grant; Immunoelectron Microscopy; Institution; Mus; Nature; Neurodegenerative Disorders; Optic Disk; Parkinson Disease; Presynaptic Terminals; Rana; Research; Research Personnel; Resources; Retinal Ganglion Cells; Source; Transgenic Organisms; United States National Institutes of Health; alpha synuclein; cellular pathology; killings; mouse model; overexpression

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. 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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 青光眼是一种神经退行性疾病，会杀死视网膜神经节细胞，是全球第二大失明原因。我们最近在多种青光眼动物模型中的数据表明，这种疾病的特征是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，我们建议对青光眼小鼠模型（DBA/2J 小鼠）的视神经乳头以及在视网膜神经节细胞中过度表达标记 Sncg 的转基因青蛙的轴突和末端进行电子和免疫电子显微镜分析。通过证明青光眼和帕金森病的常见细胞病理学，当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。