Researchers at Boston Children's Hospital have demonstrated in a live animal model that chelating zinc released after injury to the optic nerve can help protect damaged neurons in the eye and regenerate axons through the optic nerve.
Through mouse experiments, researchers reportedly found zinc levels were dramatically elevated following injury to the optic nerve. Within a few days, the zinc would move to the retinal ganglion cells, which would then begin to die off. Researchers found when they used chelators to bind the zinc, they reportedly enabled about 40 percent of the injured cells to survive for months and possibly indefinitely. Additionally, researchers observed substantial regeneration of the cells' axons.
If proven to also work in humans, researchers believe their findings could benefit patients with optic nerve injury, glaucoma, and possibly other types of nerve fiber injury within the central nervous system such as spinal cord injury.
The study was recently published in the journal Proceedings of the National Academy of Sciences.
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Source: Boston Children's Hospital