Neuroprotective role of melatonin in glaucoma

Abstract

Glaucoma is a leading cause of irreversible blindness worldwide, and causes progressive visual impairment attributable to the dysfunction and death of retinal ganglion cells (RGCs). Progression of visual field damage is slow and typically painless. Thus, glaucoma is often diagnosed after a substantial percentage of RGCs has been damaged. To date, clinical interventions are mainly restricted to the reduction of intraocular pressure (IOP), one of the major risk factors for the disease. Several concomitant factors such as elevation of synaptic glutamate and decrease in GABA levels, altered NO metabolism, and oxidative damage could significantly contribute to the neurodegeneration. Lowering IOP is often insufficient to halt or reverse the progress of visual loss, underlining the need for the development of alternative treatment strategies.Although the current management of glaucoma is mainly directed at the control of intraocular pressure, a therapy that prevents the death of retinal ganglion cells and optic nerve head fiber loss should be the main goal of treatment. Several lines of evidence strongly support that melatonin behaves as a neuroprotector in experimental animal models of various neurological and neurodegenerative disorders. In this chapter, we will consider evidence supporting that melatonin which decreases retinal glutamate synaptic levels, NO production, and oxidative damage, increases GABA synaptic levels, and prevents retinal ganglion cell and optic nerve fiber loss induced by chronic ocular hypertension, could be considered as a new therapeutic resource for the management of glaucoma.