OCTA and Glaucoma Progression in the Non-Human Primate

描述 青光眼是一组导致视网膜神经节细胞(RGC)病理性丧失且不可逆转的疾病 视力丧失。眼压升高是青光眼的主要危险因素，但一些患有青光眼的人 压力高的人永远不会得病，而压力低的人则会失明。同样，在 非人灵长类实验性青光眼模型，眼压曲线相似的动物显示 视网膜神经纤维层(RNFL)厚度丢失的程度和比率有显著差异。无论是临床还是 实验模型表明，除了眼压，青光眼还需要考虑其他因素 进步。我们假设疾病进展的可变性可以用血管因素来解释。这个 视网膜是体内代谢最多的组织之一，目前尚不清楚眼睛是否有相对较低的血管 体积，或表现出更大的血流灌注变化与眼压变化的眼睛有更大的病理风险。 此外，尽管视神经病变的眼睛血管密度降低，但尚不清楚是否存在 视网膜血管的改变是RGC丧失之前的改变。光学相干断层血管成像(OCTA) 是一种无创的三维血管灌注成像方法。然而，OCTA图像的分析 血管系统是以平板投影为基础的，在这种投影中，组织的三维性质消失了。此外，OCTA 血管血流灌注通常被认为是一种静态测量，但血管血流速度具有时间特性。为 在这个项目中，我们优化了OCTA扫描以量化血管体积和血管体积密度，并使用 顺序扫描和配准扫描，OCTA时间变异性。非人灵长类动物实验性青光眼 模型，我们将确定：1.疾病进展速度是否与基线全球和区域措施有关 血管体积/体积密度和局部OCTA时间变异性，2.是否有血管体积丢失 在视网膜内层厚度之前，3.结构和功能的变化率是否与 哪个血管的血流灌注会随着眼压的变化而改变，以及4.利用尸检组织，定义血管解剖。 (周细胞覆盖率、内皮细胞密度、毛细血管基底膜厚度/完整性) 眼部疾病与活体OCTA措施的相关性。成功完成这些目标将确定是否 用OCTA量化的血管测量可以用来确定病理风险和青光眼的发生率 进步。

DESCRIPTION Glaucoma is a group of diseases that results in a pathological loss of retinal ganglion cells (RGC) and irreversible vision loss. Increased intraocular pressure (IOP) is a major risk factor for glaucoma, but some individuals with elevated pressures never develop disease, and others with low pressures progress to blindness. Similarly, in the non-human primate experimental glaucoma model, animals with similar IOP profiles are shown to have significant differences in the extent and rate of retinal nerve fiber layer (RNFL) thickness loss. Both clinical and experimental models suggest that in addition to IOP, other factors need to be considered for glaucoma progression. We hypothesize the variability in disease progression can be explained by vascular factors. The retina is one of the most metabolic tissues in the body, and it is unknown if eyes with relatively lower vascular volume, or eyes that show greater change in perfusion with changes in IOP are at greater risk of pathology. Furthermore, although eyes with optic neuropathy have reduced vascular density, it remains unknown if there are changes in retinal vasculature that precede RGC loss. Optical coherence tomography angiography (OCTA) is a non-invasive method for three-dimensional vascular perfusion imaging. However, analysis of OCTA imaged vasculature is based on slab projections, where the three-dimensional nature of tissue is lost. In addition, OCTA vascular perfusion is often considered a static measure, but vascular flow velocity has temporal properties. For this project, we have optimized OCTA scans to quantify vascular volume and vascular volume density, and using sequential and registered scans, OCTA temporal variability. In the non-human primate experimental glaucoma model, we will determine; 1. if the rate of disease progression is related to baseline global and regional measures of vascular volume / volume density and regional OCTA temporal variability, 2. if there is loss of vascular volume prior to inner retinal thickness, 3. if the rate of structural and functional changes are is related to the extent to which vascular perfusion changes with IOP challenge, and 4. using post-mortem tissue, define vascular anatomy (pericyte coverage, endothelial cell density, capillary basement membrane thickness/integrity) in healthy and disease eyes and association with in vivo OCTA measures. Successful completion of these aims will establish if vascular measures as quantified using OCTA can be used to determine risk of pathology, and rate of glaucoma progression.