Reversible Ganglion Cell Dysfunction in Glaucoma

青光眼可逆性神经节细胞功能障碍

• 批准号: 7111872
• 负责人: VITTORIO PORCIATTI
• 金额: $ 3.19万
• 依托单位: UNIVERSITY OF MIAMI SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2004
• 资助国家: 美国
• 起止时间: 2004-12-01 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7111872
• 关键词: Reversible; Ganglion; Cell; Dysfunction; Glaucoma

DESCRIPTION (provided by applicant): Loss of sight in glaucomatous optic neuropathy is due to the death of retinal ganglion cells (RGC). Our long-term goal is to test the hypothesis that dysfunction of RGC precedes their death in early stages of glaucomatous optic neuropathy, and that vision may be spared if this dysfunction is first detected and then treated. Our immediate goal is to understand the relationships between potentially reversible functional changes and irreversible structural changes of RGC in the progression of glaucoma. Our collaborative research team combines expertise in glaucoma, visual electrophysiology, biophysics, and retinal imaging, working in a unique clinical-research setting that has a large number of patients with suspicion of glaucoma including high rates of individuals of African American and Hispanic descent. We will use non-invasive techniques that we developed to evaluate RGC function and structure - including the pattern electroretinogram (PERG) to measure potentially reversible functional changes of RGC, and Optical Coherence Tomography (OCT) to measure irreversible structural changes of RGC and their axons - in selected groups of these patients. We will also use non-invasive paradigms - suction cup to increase the intraocular pressure (IOP) and topical treatment to lower IOP - to establish whether PERG abnormalities depend on IOP. The specific aims are: 1) to identify and characterize PERG abnormalities in glaucoma suspects, 2) to understand the relationship between PERG losses and OCT losses, and 3) to understand the relationship between PERG abnormalities and induced changes in IOP. This combined, innovative approach will yield a better understanding of the pathophysiological mechanisms in the progression of glaucomatous neuropathy, may provide a rationale for treatment or prevention of glaucoma, and will develop a method to monitor the efficacy of treatment based on RGC function.

描述（由申请人提供）：glaucomatus视神经神经病的视力丧失是由于视网膜神经节细胞（RGC）死亡所致。我们的长期目标是检验以下假设：RGC的功能障碍先在青光眼视力神经病的早期死亡之前死亡，如果首先检测到此功能障碍然后治疗，则可以将视力保留下来。我们的直接目标是了解青光眼进展中RGC的潜在可逆功能变化与不可逆的结构变化之间的关系。我们的合作研究团队结合了青光眼，视觉电生理学，生物物理学和视网膜成像的专业知识，在独特的临床研究环境中工作，该环境中有大量怀疑青光眼的患者，包括非裔美国人和西班牙裔下降的高率。我们将使用我们开发的非侵入性技术来评估RGC功能和结构 - 包括模式电子图（PERG）来测量RGC的潜在可逆功能变化以及光学相干性层析成像（OCT），以测量RGC及其轴突不可逆的结构变化 - 在这些患者的选定组中。我们还将使用非侵入性范例 - 吸入杯来增加眼内压（IOP）和局部处理以降低IOP-以确定PERG异常是否取决于IOP。具体目的是：1）识别和表征青光眼嫌疑犯的佩格异常，2）了解PERG损失与OCT损失之间的关系，以及3）了解PERG异常和IOP诱发的变化之间的关系。这种结合的创新方法将更好地理解青光眼神经病进展中的病理生理机制，可以为治疗或预防青光眼提供理由，并将开发一种基于RGC功能的治疗方法来监测治疗的功效。