Table 2.
Potential strategies for preventing retinal ganglion cell death and restoring normal function
| Protection of undamaged but at-risk retinal ganglion cells and axons from noxious stimuli released by proximate damaged tissue and/or prevention of initiation of the apoptosis program |
| N-Methyl-d-aspartate (NMDA)/other excitatory amino acid mantagonists (block excitotoxicity) |
| Anti-oxidants/free radical scavengers (decrease levels of toxic moxygen radicals) |
| NO synthase inhibitors (block formation of reactive peroxynitrite from NO and superoxide) |
| Neurotrophins/growth factors |
| Ca2+ channel blockers (prevent entry of toxic levels of calcium into the cell body or axon) |
| Rescue of marginally damaged retinal ganglion cells and axons |
| Lazaroids/21-aminosteroids (block lipid peroxidation) |
| Up-regulation of anti-death genes (bcl-2, bcl-xL) |
| Anti-oxidants/free radical scavengers |
| Ca2+ channel blockers |
| NO synthase inhibitors |
| Neurotrophins/growth factors |
| Regeneration/regrowth/replacement of axons |
| Spanner neural grafts |
| Growth factors |
| Transglutaminases/interleukin-2 dimerizers/oligodendrocytotoxins |
| Neuroimmunomodulation—appropriately activated macrophages, T cells |
| Gene therapy (e.g., using viral vectors) vs. small molecule (drug) therapy to modulate the various pathways listed |
| Difficult and risks of gene and drug delivery to the posterior ocular segment |
| Duration and specificity of gene expression and drug effects whether delivery is local or systemic |