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Abstract
The retinal ganglion cell is a neuron in the RGC layer of the retina. They receive visual impulses from the photoreceptors and transmit them to the visual center via its axons forming the NFL which collect to form the optic nerve. They are varying in size, type and location. These cells are the main target of glaucoma. Glaucoma, the second leading cause of blindness worldwide, is a neurodegenerative disease which was previously thought to be an increase IOP, but this became completely different now. The relationship between IOP and glaucomatous damage is not straightforward. This disease affects the visual pathway from the NFL to the visual centers in the brain leading to various glaucomatous optic nerve changes, visual field changes, shrinkage of the LGN layers and damage to visual CNS. This occurs with or without an increased IOP. RGCs loss in glaucoma is thought to occur through apoptosis and this fact is thought to be changing. We argue that it is time to divert significant effort in glaucoma research to a detailed study of compartmentalised RGC dysfunction. It is obviously not sufficient to think of a neuron as a single entity or of glaucoma as a single type of insult. Whatever the ultimate cause of RGC loss might be, the primary event may well be the activation of one or more compartmentalised self destruct programs distally in the synapse and axon or proximally in the dendrites. RGC death may be only a secondary event and preventing apoptosis may not save vision. For vision, the most relevant clinical events may occur as soon as the axon is prevented from communicating efficiently with its target in the brain, or when the presynaptic inputs to RGC dendrites are disrupted. If so, inhibiting the axonal, dendritic or synaptic programs might slow the progress of glaucoma (particularly if IOP is also lowered and/or vascular perfusion improved). The concept of trying to prevent the autonomous axonal, synaptic and dendritic degeneration of RGCs has never been considered in glaucoma, but it is clearly important that we do consider it if we are to find effective therapies for this most debilitating and common of blinding diseases. Several mechanisms that may initiate retinal ganglion cell apoptosis in glaucoma have been proposed. These include neurotrophic factor deprivation, hypoperfusion, ischemia, glial cell activation by Nitric Oxide, glutamate excitotoxicity and abnormal immune response. Neuroprotection, in the context of glaucoma therapy, is treatment aimed at slowing or preventing neuronal death independent of IOP reduction while preserving physiologic function. The main goals of neuroprotection are blocking primary destructive events affecting RGCs or optic nerve fibers, enhancing RGC or optic nerve fiber survival mechanisms and repairing damage that occurs during the progressive, secondary stage of injury. Studies of neuroprotection initially investigated disorders of the central nervous system and results of such studies have led to some approved therapies for these conditions. Clinical trials of neuroprotective agents for glaucoma, however, are particularly difficult and challenging. However, we still can measure ocular neuroprotection or even its effect. Many techniques can be used in the clinical practice of this field like visual field testing, fMRI, evaluation of the optic disc and RNFL photographs, HRT, GDx – VCC and OCT. All these techniques provide adjunctive clinical information and have distinct advantages, including a high level of reproducibility and increased sensitivity for early glaucoma detection.