Glaucoma is a major cause of vision loss throughout the world.1-3 It represents a heterogeneous group of slow but progressive optic neuropathies that culminate in blindness. Glaucoma involves a triad of tissues comprising
Retinal ganglion cells
Trabecular meshwork Lamina cribrosa
the trabecular meshwork (TM) in the anterior chamber; the optic nerve head (ONH); and the retinal ganglion cells (RGCs) in the posterior chamber of the eye. The exact etiology of glaucoma is unclear, but the eventual death of RGCs through apoptotic mechanisms causes gradual loss of peripheral vision and eventually leads to blindness.1-3
The major risk factor of glaucoma is elevated IOP in the anterior chamber of the eye. Over time the pressure is transmitted to the back of the eye, leading to structural deformation of the posterior chamber tissues (notably the retina and ONH), constriction of retinal blood vessels leading to ischemia, and apoptotic death of RGCs, followed by axonal loss, leading to optic disc cupping/constriction and gradual loss of vision. Primary open-angle glaucoma (POAG), which is characterized by ocular hypertension, is the most common form. Normal-tension glaucoma, where the IOP is not elevated, probably has a different set of causative factors and is less-well understood, prompting the belief that vascular abnormalities around the retinal architecture causing ischemia may be more important in this disease. Genetic linkage analyses of heritable forms of glaucoma have identified 17 glaucoma loci, including six different loci for POAG (i.e., GLC1A to GLC1F), where the first glaucoma gene (MYOC; myocilin) is mapped to the GLC1A.2 PITX2, FOXC1, CYP1B1, and OPTN are additional genes associated with glaucoma but, as with the other genes mentioned, the exact linkage and mechanism(s) responsible for causing the disease are unknown.2 The largest genetic contributor to POAG identified to date is the GABRB3 locus, GLC11 on chromosome 15 (15q11-13 locus).4 However, since a curative approach to glaucoma would involve disease-modifying therapeutic agents, it is hoped that research in the ocular genetic arena would eventually lead to the discovery of such drugs in the future. POAG afflicts 1-4% of the population over 45 years, amounting to > 70 million people worldwide.2 The most prominent risk factors for POAG are ocular hypertension, age, race (African-American > Caucasian) and a family history of glaucoma.1'2 Additional risk factors are diabetes, high blood pressure, and other chronic systemic diseases.2
One major limitation is the inability to diagnose glaucoma, and currently the detection of ocular hypertension in patients is the only accepted phenotypic marker. However, since ocular hypertension itself is a 'quiet' disorder with no major measurable symptoms, patients are generally oblivious to this condition until they start to lose their peripheral vision, by which time the damage to the RGCs and retinal architecture has already progressed and is continuing to worsen. Therapeutic intervention with ocular hypotensive agents is aimed at slowing progression of visual field loss by reducing IOP.
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