SPATIAL EXTENT OF RETINAL DAMAGE

增龄和老年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 这项提议。结构和功能受损的程度 视网膜和视网膜下层内的视网膜区域将被探测。我们会 检验视网膜下沉积堆积会导致损失的假设 光感受器的功能。在这方面，我们有两个长期目标： 首先，为什么是正常衰老提供一个更好的定义，而不是 疾病的早期征兆；第二，了解疾病在 光感受器的死亡，包括视网膜下病理，如 脱离时有沉积物、新的血管膜和液体存在。我们 将确定视网膜的哪些部分受到明显的损害 局限性视网膜病变与弥漫性视网膜病变的对比研究。此信息可以 用于评估可能的预防措施，确定 治疗的局部效应、预后评估和了解 疾病过程。 为了比较结构和功能，我们使用了研究中的扫描激光器 检眼镜(SLO)。为了对视网膜下病变进行量化，我们使用红外线 成像以量化视网膜下特征的大小和位置，例如 沉积、液体堆积和视网膜下血管，甚至通过 白内障和出血。 为了量化视网膜下病变的成分，用红外线观察 成像，并验证其位置，我们使用荧光素血管造影。这个 沉积或渗出物对光感受器潜在损伤的位置 材料是量化的。视网膜下病变的构成将 通过荧光结合的模式进行探测。要评估结构 中央锥体的完整性，它们引导光线的能力将是 用Siles-Crawford I反射式测量进行量化。 黄斑中心凹视锥及周边视杆细胞的光显色功能 测量了光致变色剂的分布。我们的视网膜密度计 测量速度快，抗杂散光能力强。视觉敏感度在 选定的视网膜位置将用增量阈值进行测量。这些 将与预测的敏感度损失量进行比较 结构损坏和感光色素的量存在。 临床正常成人的横断面研究量化a) 光感受器丧失的视网膜下改变和b)模式 随着年龄的增长和年龄相关性黄斑变性的风险人群。一个 将制定正常的统计定义，以便及早发现 老年性黄斑变性。我们将比较感光色素的损失 早期和渗出性疾病的横断面结构变化 研究他们是如何受到高血压影响的。

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.