Abstract:

Glaucoma is the second leading cause of irreversible vision impairment affecting more than 70 million people worldwide with approximately 10%suffering from glaucoma-related bilateral blind (Quigley and Broman,2006). It is a multi-factorial disease that is characterized by optic nerve damage and visual field loss. Progressive loss of retinal ganglion cells (RGCs) resulting in visual field deficits is the hallmark of glaucoma. Several etiological factors seem to be involved in its pathophysiology, however the precise mechanisms leading to its development remain unclear. Some of the widely described factors that contribute to RGC loss include axonal transport failure, neurotrophic factor depletion, excitotoxicity, mitochondrial dysfunction, activation of intrinsic and extrinsic apoptotic cascade and oxidative stress (Agarwal et al., 2009). The basic mechanisms that contribute to RGC degeneration in glaucoma are presented in Figure 1. Current treatment strategies for glaucoma are limited to the reduction of intraocular pressure (IOP); however, it is clear now that the disease progression may continue despite effective IOP lowering. Search for newer modalities has led to emergence of significant data from experimental research suggesting potentially new neuroprotective strategies that may add to the arsenal of existing antiglaucoma agents.