Neuroprotection in glaucoma – what is the role of brimonidine?

Glaucoma is a chronic, multifactorial, progressive optic neuropathy and if left untreated, leads to total blindness. Damage to retinal ganglion cells and their axons in glaucoma may be caused by increased intraocular pressure, ischemia, oxidative stress, glutamate neurotoxicity, or deficiency of neurotrophic growth factor. Brimonidine is an α2-adrenergic receptor agonist, a drug commonly used to lower intraocular pressure. Its action is to inhibit the production of aqueous humor and increase its outflow by an unconventional (uveoscleral) route. The neuroprotective mechanism of action of brimonidine is believed to be related to the reduction of extracellular glutamate and blocking the activation of N-methyl-D-aspartate (NMDA) receptors, as well as the activation of brain-derived neurotrophic factor (BDNF protein) and fibroblast growth factor and their receptors, vascular modulation improving microcirculation, and regulation of cell survival and apoptosis signals. Studies have shown that 0.2% brimonidine protects retinal ganglion cells from death, not only in the mechanism of lowering IOP. The use of neuroprotective treatment of retinal ganglion cells is a promising route in glaucoma therapy.