Salient Genetic and Proteomic Pathways in Glaucoma

Glaucoma, the second leading cause of blindness worldwide is a neurodegenerative disease, with or without elevated ocular pressure, exhibiting several different phenotypic presentations, which result in progressive visual field loss after compromise of retinal ganglion cells and their axons to the optic nerve and brain. Predominant clinical glaucoma types are primary open angle, POAG, angle closure, and congenital; secondary glaucomas are: psuedoexfoliaiton, pigmentary, neovascular, traumatic, iridoendothelial, and uveitic glaucoma. In each of these types of glaucoma, genetic, epigenetic, proteomic, environmental, and mechanical forces may converge as well to cause or advance the disease. Alternatively, but not necessarily in an independent fashion, stress related pathways of oxidative stress, inflammation, infection, trauma, immune reaction, neuro-degeneration and mutant genomic products can produce deleterious misfolded proteins, antibodies, and aggregate deposits in the trabecular meshwork, TM, raise the intraocular pressure and result in optic nerve damage and loss of vision. Examining the interplay of these stress pathways with genetic, epigenetic, proteomic, environmental and mechanical forces to gain some understanding of molecular causes of glaucoma is the goal of this paper