Glaucoma is an umbrella term for a number of diseases that damage the optic nerve, which is the cluster of nerve fibers that links the retina – the light-sensitive tissue that lines the back of the eye – to the brain.
Optic nerve damage disrupts the transmission of visual signals to the brain, which can result in vision loss and blindness.
Glaucoma is most commonly caused by a buildup of eye pressure, which can damage the optic nerve. However, the precise mechanisms by which optic nerve damage occurs have been unclear, but researchers from Macquarie University in Australia may have shed some light.
The team found that a protein called neuroserpin plays a key role in retinal health, but that this protein is inactivated in glaucoma. They suggest that their findings may lead to much-needed strategies to prevent and treat the disease.
Lead study author Dr. Vivek Gupta, of the Faculty of Medicine and Health Sciences at Macquarie University, and colleagues recently published their results in the journal Scientific Reports.
Neuroserpin and glaucoma
Neuroserpin is already established as a protein that blocks the activity of an enzyme called plasmin, protecting neurons, or nerve cells, against plasmin-induced damage.
For their study, Dr. Gupta and colleagues set out to determine how neuroserpin and plasmin are affected by glaucoma.
The researchers came to their findings by analyzing retinal cells derived from humans with and without glaucoma, as well as retinas from rat models of the disease.
The analysis revealed that neuroserpin is deactivated in response to oxidative stress, which can be triggered by environmental factors such as air pollution.
Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) – which are molecules that can damage cell structures – and the body’s ability to offset their harmful effects.
Interestingly, the researchers found that neuroserpin was inactive in retinal cells from glaucoma patients and in the retinas of glaucoma rat models, which prevented the protein from inhibiting plasmin activity.
“Over a long period of time,” explains Dr. Gupta, “increased enzyme activity gradually digests the eye tissue and promotes cell death causing the adverse effects associated with glaucoma.”
It is estimated that glaucoma affects around 2.2 million adults aged 40 and older in the United States, and it is one of the country’s leading causes of vision loss and blindness.
There is currently no cure for glaucoma, but there are treatments that can help to slow progression of the disease if it is detected early enough.
Dr. Gupta and team hope that their findings will open the door to new strategies that could help to prevent or treat glaucoma.
“Ophthalmologists and vision scientists have always wondered what damages the optic nerve in the back of the eyes, which is widely observed in glaucoma,” notes study co-author Dr. Mehdi Mirzaei, of the Department of Chemistry and Biomolecular Sciences at Macquarie University.
“The breakthrough findings of this study,” he adds, “help us understand the disease mechanism and answer a key question that has eluded scientists for several years.”