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The Wlds mutation affords protection of retinal ganglion cell (RGC) axons in retinal ischemia and in inducible and hereditary preclinical models of glaucoma. We undertook the present study to determine whether the Nmnat1 portion of the chimeric protein provides axonal and somatic protection of RGCs in models of ischemia and glaucoma, particularly when localized to nonnuclear regions of the cell.

Protection of Mouse Retinal Ganglion Cell Axons and Soma from Glaucomatous and Ischemic Injury by Cytoplasmic Overexpression of Nmnat1