Researchers may have discovered a way to help the optic nerve heal following trauma by eliminating an enzyme that acts as a catalyst for inflammation.
The study, which appeared in Frontiers in Neuroscience, showed that by removing the enzyme arginase 2 (A2)—which increases following injury—neuron deaths in the retina decreased. The investigators from the Medical College of Georgia at Augusta University also found by eliminating A2, there was less degeneration of interconnecting nerve fibers.
Traditionally, few treatment options exist to help the eye recover from optic nerve crush injury, researchers noted. This is due, in part, to the lack of understanding of the complex network that causes the damage, they added.
While not much is known about A2’s normal function, it appears to be the exact opposite of arginase 1 (A1), an enzyme that helps the liver eliminate ammonia. A1 can also suppress destructive inflammation when conditions such as diabetes and glaucoma reduce blood flow to the retina. As such, when A1 levels decrease—which occurs in many eye injuries—A2 levels increase along with inflammation.
In a mouse model, researchers discovered not only did A2 increase following an injury but neurons and ganglion cells also began to die. Additionally, they found higher A2 increased the activation of glial cells—brain cells that nourish and support neurons unless they are activated.
When A2 was removed, neuron loss and never fiber degeneration lessened and glial activation was reduced.
|Xu Z, Fouda AY, Tahira L. Retinal neuroprotection from optic nerve trauma by deletion of arginase 2. Front Neurosci. December 20, 2018. [Epub ahead of print].|