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Paper presented as part of symposium. 

Abstract The Institute for Student‐AI Teaming (iSAT) addresses the foundational question:how to promote deep conceptual learning via rich socio‐collaborative learning experiences for all students?—a question that is ripe for AI‐based facilitation and has the potential to transform classrooms. We advance research in speech, computer vision, human‐agent teaming, computer‐supported collaborative learning, expansive co‐design, and the science of broadening participation to design and study next generation AI technologies (called AI Partners) embedded in student collaborative learning teams in coordination with teachers. Our institute ascribes to theoretical perspectives that aim to create a normative environment of widespread engagement through responsible design of technology, curriculum, and pedagogy in partnership with K–12 educators, racially diverse students, parents, and other community members. 

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.