The article "Age-Related Macular Degeneration, a Mathematically Tractable Disease" by Curcio et al. explores the mathematical and anatomical basis of age-related macular degeneration (AMD). The authors propose a standardized neuroanatomical nomenclature and clinical imaging approach to understand the progression of AMD. They suggest supplementing the Early Treatment of Diabetic Retinopathy Study (ETDRS) grid with an additional ring to capture high rod densities, particularly in the near-periphery region. This updated grid,称为sETDRS (supplemented ETDRS), aims to better capture the spatial distribution of photoreceptors and retinal pigment epithelium (RPE) cells, which are crucial for AMD research. The review highlights the importance of the macula lutea, a 3 mm-diameter region centered on the fovea, which is particularly vulnerable to AMD. The authors discuss the topographic relationship between foveal cone vision and the formation of high-risk drusen, as well as the distribution of rods and subretinal drusenoid deposits (SDD). They emphasize that the largest aging effects in the outer retina include accumulation of lipids in drusen, loss of choriocapillaris coverage of Bruch's membrane, and loss of rods. The article also reviews epidemiological studies that show maximal risk for drusen-related progression in the central subfield, with only one-third of this risk level in the inner ring. Vision studies report significant slowing of rod-mediated dark adaptation (RMDA) at the perimeter of the high-risk area. The authors argue that lifelong maintenance of foveal cone vision within the macula lutea leads to vulnerability in late adulthood, especially in the periphery, where rods are more densely packed. The review concludes by emphasizing the importance of adhering to the sETDRS grid and outer retinal cell populations to dissect mechanisms, prioritize research, and assist in selecting patients for emerging treatments. The authors suggest that the biology and neural geometry of AMD can inform precision prevention strategies at the population level, similar to the success in abating atherosclerotic cardiovascular disease.The article "Age-Related Macular Degeneration, a Mathematically Tractable Disease" by Curcio et al. explores the mathematical and anatomical basis of age-related macular degeneration (AMD). The authors propose a standardized neuroanatomical nomenclature and clinical imaging approach to understand the progression of AMD. They suggest supplementing the Early Treatment of Diabetic Retinopathy Study (ETDRS) grid with an additional ring to capture high rod densities, particularly in the near-periphery region. This updated grid,称为sETDRS (supplemented ETDRS), aims to better capture the spatial distribution of photoreceptors and retinal pigment epithelium (RPE) cells, which are crucial for AMD research. The review highlights the importance of the macula lutea, a 3 mm-diameter region centered on the fovea, which is particularly vulnerable to AMD. The authors discuss the topographic relationship between foveal cone vision and the formation of high-risk drusen, as well as the distribution of rods and subretinal drusenoid deposits (SDD). They emphasize that the largest aging effects in the outer retina include accumulation of lipids in drusen, loss of choriocapillaris coverage of Bruch's membrane, and loss of rods. The article also reviews epidemiological studies that show maximal risk for drusen-related progression in the central subfield, with only one-third of this risk level in the inner ring. Vision studies report significant slowing of rod-mediated dark adaptation (RMDA) at the perimeter of the high-risk area. The authors argue that lifelong maintenance of foveal cone vision within the macula lutea leads to vulnerability in late adulthood, especially in the periphery, where rods are more densely packed. The review concludes by emphasizing the importance of adhering to the sETDRS grid and outer retinal cell populations to dissect mechanisms, prioritize research, and assist in selecting patients for emerging treatments. The authors suggest that the biology and neural geometry of AMD can inform precision prevention strategies at the population level, similar to the success in abating atherosclerotic cardiovascular disease.