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Background/Objectives: To investigate macular vascular biomarkers for the detection of primary open-angle glaucoma (POAG). Methods: A total of 56 POAG patients and 94 non-glaucomatous controls underwent optical coherence tomography angiography (OCTA) assessment of macular vessel density (VD) in the superficial (SCP), and deep (DCP) capillary plexus, foveal avascular zone (FAZ) area, perimeter, VD, choriocapillaris and outer retina flow area. POAG patients were classified for severity based on the Glaucoma Staging System 2 of Brusini. ANCOVA comparisons adjusted for age, sex, race, hypertension, diabetes, and areas under the receiver operating characteristic curves (AUCs) for POAG/control differentiation were compared using the DeLong method. Results: Global, hemispheric, and quadrant SCP VD was significantly lower in POAG patients in the whole image, parafovea, and perifovea (p < 0.001). No significant differences were found between POAG and controls for DCP VD, FAZ parameters, and the retinal and choriocapillaris flow area (p > 0.05). SCP VD in the whole image and perifovea were significantly lower in POAG patients in stage 2 than stage 0 (p < 0.001). The AUCs of SCP VD in the whole image (0.86) and perifovea (0.84) were significantly higher than the AUCs of all DCP VD (p < 0.05), FAZ parameters (p < 0.001), and retinal (p < 0.001) and choriocapillaris flow areas (p < 0.05). Whole image SCP VD was similar to the AUC of the global retinal nerve fiber layer (RNFL) (AUC = 0.89, p = 0.53) and ganglion cell complex (GCC) thickness (AUC = 0.83, p = 0.42). Conclusions: SCP VD is lower with increasing functional damage in POAG patients. The AUC for SCP VD was similar to RNFL and GCC using clinical diagnosis as the reference standard. 

Common risk factors for many ocular pathologies involve non-pathologic, age-related damage to the optic nerve. Understanding the mechanisms of age-related changes can facilitate targeted treatments for ocular pathologies that arise at any point in life. In this review, we examine these age-related, neurodegenerative changes in the optic nerve, contextualize these changes from the anatomic to the molecular level, and appreciate their relationship with ocular pathophysiology. From simple structural and mechanical changes at the optic nerve head (ONH), to epigenetic and biochemical alterations of tissue and the environment, multiple age-dependent mechanisms drive extracellular matrix (ECM) remodeling, retinal ganglion cell (RGC) loss, and lowered regenerative ability of respective axons. In conjunction, aging decreases the ability of myelin to preserve maximal conductivity, even with “successfully” regenerated axons. Glial cells, however, regeneratively overcompensate and result in a microenvironment that promotes RGC axonal death. Better elucidating optic nerve neurodegeneration remains of interest, specifically investigating human ECM, RGCs, axons, oligodendrocytes, and astrocytes; clarifying the exact processes of aged ocular connective tissue alterations and their ultrastructural impacts; and developing novel technologies and pharmacotherapies that target known genetic, biochemical, matrisome, and neuroinflammatory markers. Management models should account for age-related changes when addressing glaucoma, diabetic retinopathy, and other blinding diseases. 

Précis:Capillary and neuronal tissue loss occur both globally and with regional specificity in pre-perimetric glaucoma patients at the level of the optic nerve and macula, with perifovea regions affected earlier than parafovea areas. Purpose:To investigate optic nerve head (ONH) and macular vessel densities (VD) and structural parameters assessed by optical coherence tomography angiography in pre-perimetric open angle glaucoma (ppOAG) patients and healthy controls. Materials and Methods:In all, 113 healthy and 79 ppOAG patients underwent global and regional (hemispheric/quadrants) assessments of retinal, ONH, and macular vascularity and structure, including ONH parameters, retinal nerve fiber layer (RNFL) and ganglion cell complex (GCC) thickness. Comparisons between outcomes in ppOAG and controls were adjusted for age, sex, race, BMI, diabetes, and hypertension, withP<0.05 considered statistically significant. Results:In ppOAG compared with healthy controls: RNFL thicknesses were statistically significantly lower for all hemispheres, quadrants, and sectors (P<0.001–0.041); whole image peripapillary all and small blood vessels VD were statistically significantly lower for all the quadrants (P<0.001–0.002), except for the peripapillary small vessels in the temporal quadrant (ppOAG: 49.66 (8.40), healthy: 53.45 (4.04);P=0.843); GCC and inner and full macular thicknesses in the parafoveal and perifoveal regions were significantly lower in all the quadrants (P=0.000–P=0.033); several macular VD were significantly lower (P=0.006–0.034), with the exceptions of macular center, parafoveal superior and inferior quadrant, and perifoveal superior quadrant (P>0.05). Conclusions:In ppOAG patients, VD biomarkers in both the macula and ONH, alongside RNFL, GCC, and macular thickness, were significantly reduced before detectable visual field loss with regional specificity. The most significant VD reduction detected was in the peripheric (perifovea) regions. Macular and ONH decrease in VD may serve as early biomarkers of glaucomatous disease.