Pharmacological Neuroprotection in Blinding Eye Diseases

Abstract

Pharmacological neuroprotection aims at neutralising some of the effects of the nerve-derived toxic factors, thereby increasing the ability of the spared neurons to cope with stressful conditions. Understanding of the role of extracellular calcium transport across cell membranes in modulating various intracellular signaling processes, including the initiation of the apoptotic cascade, represents part of the rationale for interest in investigating calcium-channel blockers for neuroprotection in such blinding eye diseases as glaucoma and retinitis pigmentosa. Glaucoma is a major cause of worldwide irreversible blindness. Bilateral blindness will be present in 5.9 million people with open-angle glaucoma and 5.3 million people with angle-closure glaucoma in 2020. Currently, glaucoma is recognised as an optic neuropathy and the loss of vision in this eye disease is attributed to degeneration of the axons of the retinal ganglion cells through apoptosis. Retinitis pigmentosa (RP) represents a group of progressive hereditary diseases of the retina that lead to incurable blindness and affect two million people worldwide, RP has been known to be initiated by photoreceptor apoptosis as a final common pathway at the cellular level, irrespective of gene mutations. Apoptosis can thus be considered as a therapeutic target in glaucoma and retinitis pigmentosa. This review focuses on cellular events associated with neurodegeneration due to glaucoma and retinitis pigmentosa, and discusses pharmacological agents believed to have a neuroprotective role in these diseases .It is time to conduct a randomized controlled trial to provide direct evidence of the effectiveness of specific type calcium channel blocker in glaucoma and retinitis pigmentosa. New intervention as pharmacological neuroprotection by calcium channel blockers remains an important strategy to limit the morbidity of these eye diseases representing significant health problem.

Keywords: Glaucoma, Retinitis pigmentosa, Apoptosis, Calcium channel blockers, Neuroprotection