SPATIAL EXTENT OF RETINAL DAMAGE

增龄和年龄相关性黄斑变性对光感受器的影响 功能和支持视网膜色素上皮细胞是重点 这个提议。结构和功能损伤的程度 将探测视网膜和视网膜下层内的视网膜区域。我们将 测试视网膜下沉积物的积累导致损失的假设 光感受器的功能。在这方面，我们有两个长期目标： 首先，提供一个更好的定义什么是正常老化，而不是 疾病的早期迹象;第二，了解疾病在 光感受器的死亡，包括视网膜下病变， 沉积物、新的血管膜和分离中存在液体。我们 将确定视网膜的哪些部分被明显的 良好局部化与弥漫性视网膜疾病过程。该信息可以 用于评估可能的预防措施，确定 治疗的局部效应、估计预后和了解 疾病过程。 为了比较结构和功能，我们使用了一种研究型扫描激光器， 检眼镜（SLO）。为了量化视网膜下病变，我们使用红外线 成像以量化视网膜下特征的大小和位置， 沉积物、液体积聚和视网膜下血管，甚至通过 白内障和出血。 量化视网膜下病变的组成，用红外线 成像，并验证其位置，我们使用荧光素血管造影。的 从沉积或渗出的光感受器的潜在损害的位置 材料是量化的。视网膜下病变的组成将 通过荧光结合的模式来探测。评估结构 中心锥的完整性，它们引导光线的能力将是 用反射计Stiles-Crawford I测量进行定量。 为了量化视网膜色素功能， 测量了颜料分布。我们的视网膜密度测量 测量是快速的并且抗杂散光。视觉灵敏度. 选择的视网膜位点将用增量阈值测量。这些 将与来自以下基因座的敏感性损失的预测量进行比较： 结构性损坏和存在的色素量。 临床正常成人的横断面研究量化了a） 视网膜下变化和B）整个视网膜的感光细胞损失模式 与年龄和年龄相关性黄斑变性的风险群体。一 将制定正常的统计定义，以便早期发现 老年性黄斑变性我们将比较颜料损失 和结构的变化，在早期和渗出性疾病的横断面 研究以及他们如何受到高血压的影响。

The effects of aging and age-related macular degeneration on photoreceptor function and the supporting retinal pigment epithelial cells is the focus of this proposal. The extent of structural and functional damage across retinal area within retinal and subretinal layers will be probed. We will test the hypothesis that accumulation of subretinaI deposits leads to loss of photoreceptor function. In this context we have two long-term goals: first, to provide a better definition of what is normal aging, as opposed to early signs of disease; second, to understand the role of disease in the death of photoreceptors, including subretinal pathology such as deposits, new vessel membranes, and presence of fluid in detachment. We will determine which portions of the retina are damaged by apparently well-localized vs. diffuse retinal disease processes. This information can be of use for evaluating possible preventative measures, determining the focal effects of treatment, estimating prognosis, and understanding disease processes. To compare structure with function, we use a research Scanning Laser Ophthalmoscope (SLO). To quantify subretinal pathologies we use infra-red imaging to quantify the size and location of sub-retinal features such as deposits, fluid accumulation, and sub-retinal vessels, even through cataract and hemorrhage. To quantify the composition of subretinal pathology, seen with infra-red imaging, and verify its position, we use fluorescein angiography. The location of potential damage to photoreceptors from deposited or exudative material is quantified. The composition of the subretinal pathology will be probed by the pattern of fluorescent binding. To assess the structural integrity of the central cones, their ability to direct light will be quantified with a reflectometric Stiles-Crawford I measurement. To quantify photopigment function, foveal cone and peripheral rod photopigment distribution are measured. Our retinal densitometry measurements are rapid and resistant to stray light. Visual sensitivity at selected retinal loci will be measured with increment threshold. These will be compared with predicted amounts of sensitivity loss from loci of structural damage and amount of photopigment present. Cross sectional studies of clinically normal adults quantify the a) subretinal changes and b) pattern across the retina of photoreceptor loss with aging and in groups at risk for age-related macular degeneration. A statistical definition of normal will be developed for early detection of age-related macular degeneration. We will compare the photopigment loss and structural changes in early and exudative disease in a cross-sectional study and how they are affected by hypertension.