Often a car crash or an explosion can cause optic nerve damage. Scientists have found that removing an enzyme known to favor inflammation seems to help recover.
The researchers demonstrated for the first time using mice that have undergone an optic nerve damage difficult to treat, that the elimination of the arginase enzyme 2 lowers the risk that the retinal neuron will die and prevents degeneration of the nerve fibers that bind neurons to one another and, ultimately , of the brain.
"At present, when a person suffers an optic nerve injury, we can not do much to recover the eye. We know that we can not prevent the initial damage, there will be an acute lesion, but the removal of this enzyme (A2) prevents further amplification of the initial damage, "says Ruth Caldwell, cell biology at Augusta University.
Optical nerves connect the eyes to the brain and collect the impulses that the retina generates from the light so that we can see it. There is currently no therapy to target optic nerve trauma.
Although little is known about the function of the enzyme A2, it seems to be the opposite of the enzyme A1, which helps the liver to remove ammonia. As recently discovered by specialists, A1 can suppress destructive inflammation when diabetes or glaucoma reduces blood flow to the retina. When A1 levels drop, what happens frequently when eye damage occurs, A2 levels increase, as well as inflammation and deterioration.
In the experiment the mice discovered that after elevation of the A2 enzyme levels, after the lesion, the cells of the retinal ganglion and the optic nerve began to die. Cells do not break down just after the lesion, destruction can continue for even seven days or more.
Moreover, after the A2 enzyme level is increased, the glial cells are also activated, with the role of nourishing and supporting the neurons. Once they are activated, they lose their supportive role.
After the A2 enzyme was eliminated, the situation improved: loss of neuron decreased, as well as degeneration of nerve fibers, and the number of activated glial cells decreased. There have been other signs of support, such as the increase in neurotrophic factor derived from the brain, which helps neurons and axons survive.
"We have evidence that the axons are trying to repair themselves. Neurons try to reconnect with each other and, finally, with the brain, "says Caldwell.
Specialists also observed an increase in protein 43, or GAP43, known for axon regeneration. Also, A2 elimination inhibited lesion-related growth in inflammatory-mediated immune cells, such as interleukin.
"This could also work for other problems, such as retinal damage, specific to preterm infants, and ischemic retinopathy that occurs in diabetes," says Caldwell.
When A1 levels increase, A1 decreases. Recovery from an optical injury is more effective when removing the enzyme A2.