Owsley Cynthia, Swain Thomas A, McGwin Gerald, Clark Mark E, Kar Deepayan, Curcio Christine A
Department of Ophthalmology & Visual Sciences, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Department of Epidemiology, School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama.
Ophthalmol Sci. 2023 Jan 23;3(2):100274. doi: 10.1016/j.xops.2023.100274. eCollection 2023 Jun.
We evaluate the impact of test target location in assessing rod-mediated dark adaptation (RMDA) along the transition from normal aging to intermediate age-related macular degeneration (AMD). We consider whether RMDA slows because the test locations are near mechanisms leading to or resulting from high-risk extracellular deposits. Soft drusen cluster under the fovea and extend to the inner ring of the ETDRS grid where rods are sparse. Subretinal drusenoid deposits (SDDs) appear first in the outer superior subfield of the ETDRS grid where rod photoreceptors are maximal and spread toward the fovea without covering it.
Cross-sectional.
Adults ≥ 60 years with normal older maculas, early AMD, or intermediate AMD as defined by the Age-Related Eye Disease Study (AREDS) 9-step and Beckman grading systems.
In 1 eye per participant, RMDA was assessed at 5° and at 12° in the superior retina. Subretinal drusenoid deposit presence was identified with multi-modal imaging.
Rod intercept time (RIT) as a measure of RMDA rate at 5° and 12°.
In 438 eyes of 438 persons, RIT was significantly longer (i.e., RMDA is slower) at 5° than at 12° for each AMD severity group. Differences among groups were bigger at 5° than at 12°. At 5°, SDD presence was associated with longer RIT as compared to SDD absence at early and intermediate AMD but not in normal eyes. At 12°, SDD presence was associated with longer RIT in intermediate AMD only, and not in normal or early AMD eyes. Findings were similar in eyes stratified by AREDS 9-step and Beckman systems.
We probed RMDA in relation to current models of deposit-driven AMD progression organized around photoreceptor topography. In eyes with SDD, slowed RMDA occurs at 5° where these deposits typically do not appear until later in AMD. Even in eyes lacking detectable SDD, RMDA at 5° is slower than at 12°. The effect at 5° may be attributed to mechanisms associated with the accumulation of soft drusen and precursors under the macula lutea throughout adulthood. These data will facilitate the design of efficient clinical trials for interventions that aim to delay AMD progression.
我们评估测试目标位置在评估从正常衰老到中度年龄相关性黄斑变性（AMD）转变过程中杆介导的暗适应（RMDA）时的影响。我们考虑RMDA是否会减慢，因为测试位置靠近导致高风险细胞外沉积物或由其导致的机制。软性玻璃膜疣聚集在中央凹下方，并延伸至ETDRS网格的内环，此处视杆细胞稀少。视网膜下玻璃膜疣样沉积物（SDD）首先出现在ETDRS网格的外上象限，此处视杆光感受器最多，然后向中央凹扩散但不覆盖中央凹。
横断面研究。
年龄≥60岁的成年人，其黄斑区根据年龄相关性眼病研究（AREDS）9步分级系统和贝克曼分级系统定义为正常、早期AMD或中度AMD。
每位参与者的一只眼睛，在视网膜上方5°和12°处评估RMDA。通过多模态成像确定视网膜下玻璃膜疣样沉积物的存在情况。
视杆细胞截获时间（RIT），作为5°和12°处RMDA速率的指标。
在438人的438只眼中，每个AMD严重程度组在5°处的RIT均显著长于（即RMDA较慢）12°处。各分组之间在5°处的差异大于12°处。在5°处，与早期和中度AMD中不存在SDD相比，存在SDD与更长的RIT相关，但在正常眼中不相关。在12°处，仅在中度AMD中存在SDD与更长的RIT相关，而在正常或早期AMD眼中不相关。根据AREDS 9步分级系统和贝克曼系统分层的眼睛中结果相似。
我们根据围绕光感受器地形图组织的沉积物驱动的AMD进展的当前模型探究了RMDA。在有SDD的眼中，在5°处RMDA减慢，而这些沉积物通常在AMD后期才出现。即使在没有可检测到的SDD的眼中，5°处的RMDA也比12°处慢。5°处的这种影响可能归因于与整个成年期黄斑下软性玻璃膜疣及其前体积累相关的机制。这些数据将有助于设计旨在延缓AMD进展的有效临床试验。
