In their study report, published in the online edition of the Journal of Experimental Medicine, the researchers say that their finding may result in new treatment options for the devastating disease.
Individuals with Devic's disease often experience rapid visual loss, paralysis, and loss of leg, bladder, and bowel sensation. Some lose their sight permanently.
This disease can be diagnosed by the presence of a specific self-attacking immune protein-an autoantibody referred to as NMO-IgG-in the blood.
However, it has remained unclear to date as to how that protein damages nerves and contributes to disease symptoms.
Research leader Dr. Vanda Lennon has now found that NMO-IgG sets off a chain of events that leads to a toxic build-up of a neurotransmitter called glutamate.
The researcher says that NMO-IgG binds to a protein that normally sops up excess glutamate from the space between brain cells.
In its presence, adds the researcher, this sponge-like action is blocked, allowing glutamate to accumulate.
And too much glutamate can kill the cells that produce myelin, the protein that coats and protects neurons.
The study suggests that glutamate-induced damage to nerve cells and their insulating myelin coats might account for the neurological symptoms associated with Devic's disease.
If the groups' results are confirmed in vivo, drug development could be very straightforward. herapeutic trials for glutamate blockers, created to treat other neurodegenerative diseases like Lou Gehrig's disease (or ALS), are already underway.