Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 25, 2026 2 hours, 1 minute ago
Medical News: Glaucoma is no longer seen as just an eye pressure problem. A groundbreaking scientific review is now reshaping how doctors understand this leading cause of irreversible blindness. Researchers from the Department of Ophthalmology and Visual Science at the Eye and ENT Hospital of Shanghai Medical College, Fudan University; the NHC Key Laboratory of Myopia, Fudan University; the Key Laboratory of Myopia, Chinese Academy of Medical Sciences and National Health Commission; the Shanghai Key Laboratory of Visual Impairment and Restoration; and the State Key Laboratory of Medical Neurobiology at the Institutes of Brain Science and Collaborative Innovation Center for Brain Science, Fudan University, have uncovered how the immune system may be quietly driving vision loss even when eye pressure is under control.
A new study reveals how immune overactivation inside the eye may silently drive glaucoma-related blindness
even when eye pressure is controlled.
Glaucoma Is More Than High Eye Pressure
For decades, glaucoma treatment has focused almost entirely on lowering intraocular pressure. While pressure remains a major risk factor, many patients continue to lose vision despite achieving their target pressure. Even more puzzling, some people develop glaucoma despite having “normal” eye pressure.
The new research shows that glaucoma behaves much like other brain diseases such as Alzheimer’s or Parkinson’s. Instead of being just a mechanical issue, it appears to involve chronic inflammation inside the eye. This inflammation damages retinal ganglion cells, the nerve cells responsible for carrying visual information from the eye to the brain.
The Dangerous Immune Loop Inside the Eye
The study highlights three key immune players: the complement system, the NLRP3 inflammasome, and microglia. While these terms may sound technical, their roles are easier to understand.
The complement system normally helps the body clear damaged cells. But in glaucoma, it becomes overactive. It begins tagging stressed but still living nerve connections for destruction. This leads to unnecessary pruning of important nerve pathways.
The NLRP3 inflammasome acts like a danger sensor inside cells. When triggered by stress signals such as reduced oxygen, mitochondrial damage, or chemical distress signals like ATP, it releases inflammatory chemicals including IL-1β and IL-18. These substances worsen inflammation and further injure nerve cells.
Microglia, the immune cells of the retina, sit at the center of this process. Early on, they may help clean up debris. However, under chronic stress, they shift into a harmful mode. They release inflammatory chemicals, remove still-viable nerve cells, and amplify damage. This
Medical News report highlights how these three systems form a self-reinforcing loop. Complement activation stimulates inflammasome activity. Inflammasome chemicals increase complement production. Microglia respond to both and escalate the damage.
Energy Crisis and Aging Mak
e Things Worse
The researchers also explain how energy failure contributes to disease progression. In glaucoma, nerve cells suffer from mitochondrial dysfunction, reducing their ability to produce ATP, the cell’s energy currency. At the same time, stressed cells release ATP outside the cell, which acts as a distress signal and further activates inflammation.
Aging intensifies this immune sensitivity. Older immune cells become more reactive, a process sometimes called “inflammaging.” Conditions like diabetes, vascular instability, and oxidative stress further prime the system for chronic inflammation.
Toward Immune-Based Precision Treatment
The most exciting part of the review is its proposal for immune-based precision therapy. Instead of treating all glaucoma patients the same, doctors could one day classify patients based on their immune profile. Some may have complement-dominant disease. Others may show inflammasome-driven inflammation. Still others may have microglia-dominant degeneration.
Targeted treatments could include complement inhibitors, inflammasome blockers, IL-1 pathway drugs, or therapies that reprogram microglia into protective states. This personalized strategy could help patients who continue to worsen despite well-controlled eye pressure.
Conclusion
The findings strongly suggest that glaucoma is not simply a pressure disorder but a complex neuroimmune disease driven by a self-perpetuating inflammatory circuit. By identifying the complement–inflammasome–microglia axis as a central mechanism, the researchers provide a powerful new framework for understanding why vision loss can continue even after pressure is reduced. Most importantly, the study opens the door to immune-targeted therapies that could transform glaucoma care from pressure control alone to true neuroprotection, offering renewed hope to millions at risk of blindness.
The study findings were published in the peer reviewed journal: Life.
https://www.mdpi.com/2075-1729/16/3/368
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