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/ Health News / 2008 / October 2008 / October 7, 2008 Neurotransmitter defect behind autoimmune disease uncovered |
Sack lunches may not provide adequate nutrients to preschooler
Packing lunch for your child might not be a good idea, for a new study has found that sack lunches may not regularly provide adequate nutrients for the growth and development of young children. ANI
Health-monitoring system helps maintain older adults well-being
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New drug shows potential to treat angina, other cardiac problems
A compound, designed to prevent chest pains in heart patients, could act as a drug to treat angina and possibly other cardiac pathologies, according to a study on animals. ANI
Researchers at the Mayo Clinic in Rochester, Minnesota, say that they have uncovered a neurotransmitter defect that may trigger Devics disease, a potentially blinding neurological disorder that is often confused with multiple sclerosis.
Washington, October 7 : Researchers at the Mayo Clinic in Rochester, Minnesota, say that they have uncovered a neurotransmitter defect that may trigger Devic's disease, a potentially blinding neurological disorder that is often confused with multiple sclerosis.
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.
ANI
