Glaucoma, often referred to as the “silent thief of sight,” is the leading cause of permanent blindness, affecting over 80 million people worldwide, with many others undiagnosed. This condition causes gradual damage to retinal ganglion cells (RGCs), the neurons that transmit visual information from the eye to the brain. While current treatments focus on lowering intraocular pressure (IOP), many patients still lose vision. Here, scientists explain the science behind glaucoma and explore new ideas for preventing its effects by protecting RGCs.*

How Glaucoma Damages Retinal Ganglion Cells

RGCs are crucial for vision, as they connect the eye to the brain. Beyond helping us see, they regulate other functions, like controlling how our eyes respond to light. In glaucoma, these cells are harmed by factors like:

• Aging,  
• Genetics, and 
• High IOP harms these cells. 

Until recently, scientists thought RGCs were either fully functional or permanently damaged. Now they know these cells can experience a “stressed” phase before dying, which offers a chance to save them.

Damage Happens in Stages

In glaucoma, RGC damage doesn’t happen all at once. Different parts of a cell—like the axons, dendrites, and soma (cell body)—get damaged at different times. Early damage in the axons, for instance, might not show symptoms until the damage is severe. This gradual progression makes it hard to catch glaucoma early. Researchers believe treatments targeting specific parts of the cell could slow or even stop the disease.

Eye Cells Need Energy 

The retina, a thin layer of tissue at the back of the eye, uses a lot of energy to process visual information. RGCs rely on mitochondria, the powerhouses of the cell, to produce energy. When mitochondria don’t work properly, RGCs can’t function or survive. Studies have shown that problems with mitochondria, like reduced energy production, can worsen glaucoma.

New Treatments for Energy Imbalances

Scientists are exploring and testing therapies to boost mitochondrial health and energy production, such as: 

• Nicotinamide (a form of vitamin B3), which helps RGCs produce more energy and has been successful in animal studies,
• Antioxidant-rich diets, and
• Drugs that improve mitochondrial function. 

Clinical trials are underway to see if these therapies could work for humans.

Inflammation’s Role in Glaucoma

Inflammation and RGC Damage

Glaucoma causes inflammation in the retina, which worsens the damage to RGCs. Normally, glial cells support and protect neurons, but in glaucoma, they become overactive and release harmful chemicals. This creates a toxic environment that speeds up RGC death. Scientists have also found that inflammation starts early in the disease, sometimes before major cell loss occurs.

Fighting Inflammation for Neuroprotection

Reducing inflammation has shown promise in saving RGCs. Some substances like minocycline and valproic acid have been shown to slow vision loss by lowering inflammation levels in animal studies, along with more targeted procedures like gene deletion and treatments to block specific pathways related to the immune system. 

Researchers are now working on ways to apply these discoveries to humans, offering hope for new, vision-saving treatments.

A Future of Hope

Glaucoma research is making exciting progress. By better understanding how the disease works, scientists are developing new ways to protect RGCs, focusing on:

• Energy production, 
• Inflammation reduction, and 
• Other key processes. 

While challenges like early detection and personalized treatments remain, these advancements bring hope for therapies that could go beyond controlling IOP, and directly tackle the root causes of glaucoma.

*Tribble, J.R., Hui, F., Quintero, H., El Hajji, S., et al. (Neuroprotection in glaucoma: Mechanisms beyond intraocular pressure lowering. Molecular Aspects of Medicine. Retrieved from    https://www.sciencedirect.com/science/article/pii/S009829972300033X 

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