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Given that glaucoma is a disease of the central nervous system, there must be greater emphasis and focus on developing intraocular pressure-independent therapies. In addition, scientific research investigating the role of sustained drug delivery is critical for advancing the field. Exciting innovation will require close collaboration and full integration of clinical and basic research efforts. Thus, translational research advances in neuroprotection may lead to future development of truly revolutionary therapies for glaucoma (e.g., neuroregeneration)., (Copyright © 2013 Canadian Ophthalmological Society. Published by Elsevier Inc. All rights reserved.)

Most optic neuropathies do not have effective treatments. Examples are ischemic optic neuropathy, Leber hereditary optic neuropathy, optic neuritis, and traumatic optic neuropathy. In some cases, the pathophysiology of the optic nerve injury is not fully understood. For example, while the demyelinative aspects of optic neuritis have been studied, the mechanism by which the axonal loss occurs is less apparent. In other cases, although the pathophysiology of the optic neuropathy may be understood, there is difficulty treating the disease, for example, with traumatic optic neuropathy. In response to this therapeutic dearth, the concept of neuroprotection has arisen. Neuroprotection is a therapeutic paradigm for preventing death of neurons from injury and maintaining function. In optic neuropathies, the corresponding neuron is the retinal ganglion cell. These cells are unable to divide, and optic neuropathies irrevocably result in their death; therefore, the primary target of neuroprotection are retinal ganglion cells and their axons. This review emphasizes that most optic neuropathies are axonal and thus good targets for neuroprotection.

The glaucomas are a group of ocular diseases characterized by progressive optic nerve damage and visual loss. Although there is good laboratory evidence for glaucoma neuroprotection by several drugs, the evidence from randomized clinical trials is lacking.

There is an abundance of evidence from recent randomized clinical trials showing that lowering the IOP is beneficial to the optic nerve and visual field. Setting and achieving a target IOP range is in keeping with evidence-based medicine. The benefits of reaching this target must be weighed against the risks of the treatment itself. Target IOP is a dynamic concept, needing constant reevaluation. What is lacking are established guidelines for determining the target IOP range that can be used in general ophthalmology practice.