Retina Society 2026:
Margherio Award — Outer Segment Thinning and Polygenic Risk Interact to Predict AMD
The Margherio Award at this year’s Retina Society annual meeting (September 25, 2026) was awarded to Dr. Seyedeh Maryam Zekavat, MD PhD from Mass Eye and Ear for “Photoreceptor Outer Segment Thinning and Polygenic Risk Interact to Predict Future AMD Risk: Evidence from the UK Biobank.” The talk built on her prior work, which segmented nine OCT retinal layers and found that photoreceptor segment thinning was the layer most predictive of incident AMD. Here, the team split the photoreceptor segment into its inner and outer components across 50,149 UK Biobank participants (818 incident AMD cases, median 13.6-year follow-up) to ask which component carries the signal, and whether it interacts with genetic risk to influence AMD risk.
The answer: outer segment (OS), not inner segment (IS), thickness drives the association (~30% increased AMD risk per standard deviation decrease in outer segment thickness), making photoreceptor OS thickness the second-strongest predictor of incident AMD behind only a genome-wide polygenic risk score (PRS). OS thickness and the AMD PRS interacted significantly, with individuals in the highest PRS quartile and lowest OS quartile carrying more than 4-fold increased risk compared to those in the low-risk group. The findings held up in 444 manually-graded images, where eyes with geographic atrophy showed roughly 2 standard deviation lower OS thickness in comparison to individuals without an AMD diagnosis. Locus-level analyses tied the OS-PRS interaction specifically to CFH and C3 variants, pointing to the complement pathway, and drawing a connection to pegcetacoplan (Syfovre), the FDA-approved complement inhibitor for geographic atrophy.
Overall, this work provides a more anatomically precise and mechanistically informative account of how OCT-derived structural imaging and genomic risk jointly predict AMD. Dr. Zekavat closed by calling for the need for future longitudinal, high-resolution OCT studies to track OS thickness over time in diverse patient cohorts.
Retina Society 2026:
Fellowship research award: Rethinking Diabetic Choroidopathy: Is Altered Blood Flow a Fundamental Driver?
The 2026 Fellow Research Award at this year’s Retina Society annual meeting was awarded to Dr. Woojung Chae, MD from South Korea for “Flow-Dependent Vascular Instability and Inflammation in Diabetic Choroidopathy: Implications for Therapeutic Targeting.” Diabetic choroidopathy (DC) has historically received far less attention than diabetic retinopathy and diabetic macular edema. Yet the choroid plays a critical role in supporting the outer retina and photoreceptors, and abnormalities in the choroidal circulation may have important consequences for retinal structure and visual function. Despite its potential importance, the mechanisms underlying diabetic choroidal vascular dysfunction remain poorly understood.
Dr. Chae’s research has focused on understanding how changes in the choroidal circulation may contribute to visual dysfunction in patients with diabetes. Using multimodal imaging and functional assessments, including optical coherence tomography, indocyanine green angiography, OCTA, FAF, and microperimetry, the team has investigated the structural and functional consequences of diabetic choroidal abnormalities.
A central question emerging from this work is whether abnormal blood flow is simply a consequence of diabetic vascular disease or whether it may actively contribute to the development of diabetic choroidopathy.
In her recent study, she addressed this question using complementary human and experimental approaches. Analysis of human diabetic choroidal tissue suggested a role for altered blood flow in diabetes, and they subsequently validated these findings in experimental diabetic models. This approach allowed the team to move beyond the observation of vascular abnormalities and investigate how altered blood flow may directly affect the choroidal vasculature.
The findings suggest that blood flow provides an important mechanical signal for maintaining the health and stability of choroidal endothelial cells. When this flow-dependent signaling is disrupted, endothelial junctional integrity is compromised and vascular inflammatory responses are increased. Conversely, modulating this signaling improved several features of diabetic choroidal vascular dysfunction, including vascular dilation, leakage, and inflammation.
These findings raise the possibility that altered blood flow may not simply be a feature of diabetic choroidopathy, but may represent an upstream driver linking multiple pathological manifestations of the disease. Rather than viewing vascular dilation, leakage, and inflammation as independent abnormalities, these findings suggest that they may arise, at least in part, from a common disturbance in the interaction between blood flow and the vascular endothelium.
This concept may provide a new framework for understanding diabetic choroidopathy and, more broadly, other choroidal disorders characterized by vascular inflammation, congestion, and impaired vascular homeostasis. Ultimately, understanding and modulating the mechanisms that maintain healthy interactions between blood flow and the vascular endothelium may open new therapeutic possibilities for these challenging choroidal diseases.
