Therapeutic potentials of aspirin in glaucomatous optic neuropathy

Abstract

Glaucoma is a common blinding disease worldwide. Although traditionally considered as a disease of elevated intraocular pressure, it is now clear that glaucoma is primarily a distinctive optic neuropathy with many proposed pathogenic mechanisms. Impaired blood flow resulting in ischemia has been proposed to be involved in the retinal ganglion cell loss seen in glaucoma. Aspirin might improve optic nerve head perfusion by stabilizing microcirculatory flow. Evidence also indicates that apoptosis may be the final common pathway for ganglion cell death in glaucoma. Aspirin has been shown to exhibit neuroprotective properties. Prostaglandins play an important role in the regulation of intraocular pressure. Aspirin is well known to inhibit cyclooxygenase mediated prostaglandin synthesis. The NSAID-inhibition of PGs synthesis up-regulates the concentration prostaglandin receptors in retinovascular tissues. Based on the body of evidence implicating ocular blood flow disturbances, apoptotic cell death, and also the role of prostaglandins in the pathogenesis of glaucoma we hypothesize that aspirin could be potentially useful drugs in the treatment of glaucoma. Hypothetical pathophysiologic mechanisms explaining potential beneficial effects of aspirin on glaucomatous optic neuropathy include: increasing optic nerve blood flow, preventing retinal ganglion cell death through neuroprotective mechanisms, and upregulating prostaglandin receptors.