Glaucoma is the leading cause of blindness for people over 60 years old. It is a group of diseases that occur when aqueous humour is unable to flow out of the eye properly, causing an increase in fluid pressure in the eyes, which cause ocular hypertension and damage the optic nerve over time. The flow of aqueous humour can be disrupted either by a partial or full block of its drainage canal or an excess production of the fluid, and the chronic increase in intraocular pressure (IOP) leads to a gradually progressive loss of the visual field and a slow degeneration of the optic nerve (Boyd, 2015). Glaucoma is known to cause widespread loss of retinal ganglion cells (RGCs) over time. As pressure on the optic nerve increases, RGCs are thought to be directly traumatized, which leads to shrinkage and death, and
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The glial cells formed a mesh network, extending posteriorly from the entrance of the scleral canal, through which the axons passed; the network ended before the myelin sheath of most axons. The results equally supported the hypothesis that the glial lamina was an important site of axon trauma. Neurons in the nerve fibre layer, in the prelaminar region (optic nerve head), and at the exit point of the lamina were analyzed, and damaged axon segments, similar to dystrophic neurites of other conditions, were readily detected in the lamina, but were rarely found in the prelaminar region, and did not appear in the nerve fiber layer. Cyan fluorescent protein (CFP) marking also revealed that most early damage, in the form of discrete and focal swellings, was localized in the lamina. Additionally, the data suggested that axons were insulted to different degrees; severe insults would cause a rapid Wallerian degeneration, where the entire axon segment rapidly degenerates distal to a lesion, and lesser insults caused minor axonal damage (Howell, et al.,
The glial cells formed a mesh network, extending posteriorly from the entrance of the scleral canal, through which the axons passed; the network ended before the myelin sheath of most axons. The results equally supported the hypothesis that the glial lamina was an important site of axon trauma. Neurons in the nerve fibre layer, in the prelaminar region (optic nerve head), and at the exit point of the lamina were analyzed, and damaged axon segments, similar to dystrophic neurites of other conditions, were readily detected in the lamina, but were rarely found in the prelaminar region, and did not appear in the nerve fiber layer. Cyan fluorescent protein (CFP) marking also revealed that most early damage, in the form of discrete and focal swellings, was localized in the lamina. Additionally, the data suggested that axons were insulted to different degrees; severe insults would cause a rapid Wallerian degeneration, where the entire axon segment rapidly degenerates distal to a lesion, and lesser insults caused minor axonal damage (Howell, et al.,