Neuroprotection in the treatment of glaucoma – A focus on connexin43 gap junction channel blockers

• Conventional and novel IOP-lowering glaucoma medications are briefly described.
• Neuroprotection is then introduced as novel strategy for glaucoma treatment.
• Neuroprotectants can prevent RGC loss and therefore preserve the patient’s vision.
• Cx43 gap junction/hemichannel blockers are discussed as novel neuroprotective agents.
• Cx43 channel modulators can block both neuronal and inflammatory pathogenic cascades.

Glaucoma is a form of optic neuropathy and a common cause of blindness, affecting over 60 million people worldwide with an expected rise to 80 million by 2020. Successful treatment is challenging due to the various causes of glaucoma, undetectable symptoms at an early stage and inefficient delivery of drugs to the back of the eye. Conventional glaucoma treatments focus on the reduction of elevated intraocular pressure (IOP) using topical eye drops. However, their efficacy is limited to patients who suffer from high IOP glaucoma and do not address the underlying susceptibility of retinal ganglion cells (RGC) to degeneration. Glaucoma is known as a neurodegenerative disease which starts with RGC death and eventually results in damage of the optic nerve. Neuroprotective strategies therefore offer a novel treatment option for glaucoma by not only preventing neuronal loss but also disease progression. This review firstly gives an overview of the pathophysiology of glaucoma as well as current treatment options including conventional and novel delivery strategies. It then summarizes the rational for neuroprotection as a novel therapy for glaucomatous neuropathies and reviews current potential neuroprotective strategies to preserve RGC, with a focus on connexin43 (Cx43) gap junction channel blockers.

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