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 block inappropriate immune responses.
Later in the course of disease, Steinman says, a drug that blocks
glutamate could be used to protect against nerve damage and myelin destruction.
