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Glaucomatous optic neuropathy (GON) associated with different forms of glaucoma and chronic ocular hypertension (cOHT) is characterized by progressive loss of retinal ganglion cells and their axons in the optic nerves that project to the brain to transmit visual information. The resultant thinning of the optic nerves cause loss of peripheral vision, which if not halted or slowed, can lead to irreversible blindness. Whilst the precise triggering insult(s) for the primary open angle glaucoma (POAG), the most prevalent of the glaucomas, remains unknown, the most prominent risk factors include elevated intraocular pressure, increasing age, African-American heritage (genetic predisposition), family history, low cerebral spinal/intracranial pressure, and vascular dysfunctions within the retina. However, whilst reduction of IOP by topical ocularly administered medications is the first-line therapeutic approach to address cOHT / POAG, surgical procedures and aqueous humor drainage devices are also useful means to lower IOP. It is hoped that the intense research into mechanisms underlying neurodegeneration has the potential to lead to discovery of potential neuroprotective and neuroregenerative agents s and technologies including novel sustained drug delivery platforms, gene therapy, cell therapy, physical support systems, food-derived nutrient treatments, neurostimulation via optogenetic, electrical and sonogenetic tools, yielding suitable treatments to treat cOHT / POAG and the attendant GON.

Neuropathology and Therapeutics Addressing Glaucoma, a Prevalent Retina-Optic Nerve-Brain Disease that Causes Eyesight Impairment and Blindness