Glaucoma is a disorder that pertains to a group of eye conditions that damages the optic nerve. It is characterized by the dysfunction and loss of retinal ganglion cells (RGCs). A retinal ganglion cell (RGC) is a type of neuron located near the inner surface (the ganglion cell layer) of the retina of the eye. The RGC carries visual information from the eye to the brain.
Glaucoma is a leading cause of visual loss. It is a complex disease that is characterized by the loss of retinal ganglion cells (RGCs) and their axons. Major risk factors include older age and higher intraocular pressure (IOP). Current treatments act to lower IOP but are not effective in many cases. Although glaucoma is estimated to affect over 60 million people, more work is needed to understand the molecular mechanisms that damage RGCs.
There are four major types of Glaucoma:
- Open-angle (chronic) glaucoma: The most common type of glaucoma and occurs over time. The IOP pushes on the optic nerve.
- Angle-closure (acute) glaucoma: Treated as an emergency, this type of glaucoma occurs when the exit of the aqueous humor fluid is suddenly blocked. This causes a quick, severe, and painful rise in the pressure in the eye.
- Congenital glaucoma: Present at birth and is caused by abnormal eye development.
- Secondary glaucoma: Caused by drugs, disease, and trauma.
Treatment for glaucoma involves relieving the intraocular pressure on the optic nerve. Depending on the type of glaucoma, treatment may be through eye drops, laser therapy (iridotomy), or surgery.
Video: What is Glaucoma?
Glaucoma is one of the leading causes of vision loss and blindness worldwide which is estimated at 60 million. Glaucoma is the second most common cause of blindness in the United States. In glaucoma patients, the optic nerve, which relays information from the eye to the brain, is damaged, though the molecular cause of nerve damage is unclear.
Dr. Simon John, from Tufts University in Boston, and colleagues specifically wanted to understand the earliest events that lead to optic nerve damage in glaucoma. Using a mouse model of the disease, the researchers showed that inflammatory immune cells called monocytes cross blood vessels and invade the optic nerve. This resulted in proinflammatory monocytes entering the optic nerve prior to detectable neuronal damage. A 1-time x-ray treatment prevented monocyte entry and subsequent glaucomatous damage. A single x-ray treatment of an individual eye in young mice provided that eye with long-term protection from glaucoma but had no effect on the contralateral eye.
Localized radiation treatment prevented detectable neuronal damage and dysfunction in treated eyes, despite the continued presence of other glaucomatous stresses and signaling pathways. Injection of endothelin-2, a damaging mediator produced by the monocytes, into irradiated eyes, combined with the other glaucomatous stresses, restored neural damage with a topography characteristic of glaucoma. Together, these data support a model of glaucomatous damage involving monocyte entry into the optic nerve.
It was shown that mice treated with the single X-ray treatment in eyes prior to the onset of glaucoma were protected from developing the disease later in life. Through an unknown mechanism, the X-ray treatment prevented neuroinflammation and allowed mice to avoid glaucoma development, even in the presence of other risk factors. Continuing research by the John team will examine why the X-ray treatment effectively blocked glaucoma in the mouse model system and if this strategy might someday be adapted to prevent glaucoma in humans.
RELATED LINKS
Journal of Clinical Investigation
Tufts University
Howard Hughes Medical Institute
Glaucoma
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