
ALT Disease-specific upstream mechanisms converging on a shared optic nerve injury cascade. Four optic neuropathy contexts, open-angle glaucoma, non-arteritic anterior ischemic optic neuropathy, optic neuritis, and traumatic optic neuropathy, are shown with their early pathological mechanisms. Despite distinct upstream etiologies, all four pathways converge on a common injury cascade involving retinal ganglion cell (RGC) death signaling, metabolic collapse, reactive gliosis with extracellular matrix remodeling, and axonal transport failure. Surviving RGC axons are then subject to compounding extrinsic and intrinsic blocks, ultimately resulting in vision loss through disruption of the retina, lateral geniculate nucleus, and V1 circuit.

ALT Disease-specific upstream mechanisms converging on a shared optic nerve injury cascade. Four optic neuropathy contexts, open-angle glaucoma, non-arteritic anterior ischemic optic neuropathy, optic neuritis, and traumatic optic neuropathy, are shown with their early pathological mechanisms. Despite distinct upstream etiologies, all four pathways converge on a common injury cascade involving retinal ganglion cell (RGC) death signaling, metabolic collapse, reactive gliosis with extracellular matrix remodeling, and axonal transport failure. Surviving RGC axons are then subject to compounding extrinsic and intrinsic blocks, ultimately resulting in vision loss through disruption of the retina, lateral geniculate nucleus, and V1 circuit.

























