New MS Treatment May Have Potential For ALS
Date : Tue, 28 Dec 1999 08:01:55 -0800 (PST)
NEW YORK, Dec 27 (Reuters Health) -- Three studies released on Monday shed new light on the cause of multiple sclerosis (MS) and point to a potential new treatment for the disease.
More than one million people worldwide suffer from MS, which is characterized by muscle weakness, paralysis, slurred speech and vision problems.
Two of the three studies concerned a drug that blocks glutamate, a chemical that normally transmits information from one nerve cell to another. Levels of glutamate have been found to be increased in patients with MS.
In mice with an MS-like illness, a drug that blocked glutamate was found to prevent nerve damage and destruction of the myelin sheath, the fatty protective substance that covers nerves. Such damage is the hallmark of the human form of MS.
The toxic effects of glutamate have "been accepted as a mechanism in a lot of neurodegenerative diseases and acute brain damage like stroke," Dr. Peter Werner of Albert Einstein College of Medicine, in New York, said in a telephone interview with Reuters Health.
Blocking the receptors that recognize glutamate is already an experimental strategy used to help prevent brain damage caused by stroke, epilepsy and illnesses such as Parkinson's disease.
"What we have shown now is that this mechanism, at least in this animal model, is also present" in MS, Werner added.
According to a report in the January issue of Nature Medicine, Werner and colleagues blocked glutamate receptors in mice by administering an experimental drug known as NBQX. This treatment substantially reduced nerve damage and myelin destruction in the animals, without adversely affecting the immune system.
Werner believes that the use of such antagonists, or blocking agents, may prove to be effective against MS.
"The hope is that eventually we will be able to use glutamate antagonists, which are currently in clinical testing for stroke, to ameliorate the damage in MS, but that is still years away," he told Reuters Health.
Separately in Nature Medicine, Dr. Lechoslaw Turski and colleagues from University College London in the United Kingdom report independent results of the use of NBQX, which corroborate the results of the New York team's experiments.
Elsewhere in the journal, scientists from the US and Germany report a greater understanding of why the immune system destroys the myelin sheath in MS. Dr. Ludger Klein of the Dana Farber Cancer Institute in Boston, Massachusetts, and colleagues found that in some mice, a process called tolerance goes awry and the animals are unable to distinguish their own proteins from foreign ones.
In such animals, fragments of myelin gene are mistakenly presented to immune cells, which then attack and destroy the protein. The same thing may occur in humans, the researchers speculate.
In a News and Views article, Dr. Lawrence Steinman of Stanford University
in California foresees the day when drugs such as Copaxone, which block
the presentation of myelin fragments to the immune system, are used early
in the course of MS to blomewhere!
SOURCE: Nature Medicine 2000;1:15-16,56-67.