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Background  Early challenges to axonal physiology, active transport, and ultrastructure are endemic to age-related neurodegenerative disorders, including those affecting the optic nerve. Chief among these, glaucoma causes irreversible vision loss through sensitivity to intraocular pressure (IOP) that challenges retinal ganglion cell (RGC) axons, which comprise the optic nerve. Early RGC axonopathy includes distal to proximal progression that implicates a slow form of Wallerian degeneration. In multiple disease models, including inducible glaucoma, expression of the slow  Wallerian degeneration  ( Wld  S ) allele slows axon degeneration and confers protection to cell bodies.    Methods  Using an inducible model of glaucoma along with whole-cell patch clamp electrophysiology and morphological analysis, we tested if  Wld  S  also protects RGC light responses and dendrites and, if so, whether this protection depends upon RGC type. We induced glaucoma in young and aged mice to determine if neuroprotection by  Wld  S  on anterograde axonal transport and spatial contrast acuity depends on age.    Results  We found  Wld  S  protects dendritic morphology and light-evoked responses of RGCs that signal light onset (αON-Sustained) during IOP elevation. However, IOP elevation significantly reduces dendritic complexity and light responses of RGCs that respond to light offset (αOFF-Sustained) regardless of  Wld  S . As expected,  Wld  S  preserves anterograde axon transport and spatial acuity in young adult mice, but its protection is significantly limited in aged mice.    Conclusion  The efficacy of  Wld  S  in conferring protection to neurons and their axons varies by cell type and diminishes with age.

Neuroprotection by WldS depends on retinal ganglion cell type and age in glaucoma