Abstract
To date, intraocular pressure (IOP) control regulated in the anterior segment remains the target of all approved glaucoma treatments. Therapies directly targeting retinal ganglion cells (RGCs) are still major unmet goal, especially as lowering IOP is frequently not enough to prevent vision loss and blindness in glaucoma. While the exact process by which RGC apoptosis occurs in human glaucoma patients remains obscure and may differ among subsets of patients, many potential mechanisms have been proposed and studied, including direct barometric damage, axoplasmic flow obstruction, oxidative stress, inflammation, vascular dysregulation, synapse and/or dendrite retraction, and mitochondrial dysfunction. While neuroprotective agents are not yet approved for clinical practice, the field has leaped forward in recent years with the identification of several agents with compelling data on neuroprotective or neuroenhancing properties when tested in preclinical models or in limited human studies. Namely:
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