Glaucoma is a leading cause of blindness worldwide. Vision loss from glaucoma occurs when axons in the optic nerve become damaged and can no longer carry visual information to the brain.
Glaucoma is most often treated by lowering pressure in the eye with drugs, laser surgery, or traditional surgery. However, these treatments can only preserve remaining vision; they don’t improve or restore vision that already has been lost due to glaucoma.
The nervous system is divided into the peripheral and the central systems. Damaged peripheral nerves, in your arm for example, can regenerate after injury. However, the optic nerve and the spinal cord are in the central nervous system and unfortunately cannot regenerate after injury. This is why vision loss from glaucoma, like paralysis from spinal cord injury, is permanent. The unique cellular environment of nerve cells in the central nervous system may be why regeneration is prevented.
One strategy to encourage nerve fiber growth is to remove inhibitory factors in the cellular environment. Researchers hope to prevent expression of molecules that suppress axon growth using molecular biology techniques. For example, antibodies may be introduced to block the inhibition and allow nerve fibers to re-grow. Other strategies are in development as well:
Researchers have made great progress in understanding the process of optic nerve degeneration and regeneration in glaucoma. Molecular factors have been identified for nerve fiber growth in the central nervous system. New strategies to prevent scar formation and guide nerve fibers are being developed using nanotechnology, gene therapy, and stem cells. The next challenges are to optimize nerve regeneration and test whether it restores functionally meaningful levels of vision for glaucoma patients. This article is based on a recent “Innovations in Glaucoma” Webinar produced by Glaucoma Research Foundation: http://www.glaucoma.org/news/podcasts/audio-podcasts.php
http://www.sciencedaily.com/ Science Daily
http://www.sciencedaily.com/releases/2015/12/151216150620.htm Original web page at Science Daily