**1. Introduction**

Glaucoma is a distinctive group of optic neuropathies characterized by progressive degener‐ ation of neuronal tissue due to death of retinal ganglion cells, with accompanying gradual visual field loss. [1, 2] It is the leading cause of irreversible blindness worldwide [3] and complex genetic and environmental risk factors have been implicated in its progression. [4-7] Neuroprotection for glaucoma refers to any intervention that aims either to prevent op‐ tic nerve damage and retinal ganglion cell death or to preserve already diseased neuronal tissue and its function, with the ultimate goal of maintaining vision. Thus, neuroprotective agents can be thought of as pharmacological antagonists of intracellular injury and death pathways.

Agents that lower the intra-ocular pressure (IOP) have been shown to slow glaucoma pro‐ gression in several controlled clinical trials and even arrest the progression in some cases [8-10], yet their effectiveness is limited in preventing retinal ganglion cell loss. Retinal gan‐ glion cell damage in glaucoma is not confined to the neurons that are insulted primarily, but neighboring neurons are injured secondarily as well. [11] Therefore, efforts that focus on discovering alternative therapeutic approaches independent of IOP reduction have placed neuroprotective treatment modalities at the frontiers of glaucoma research.
