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Subject:
From:
Mariana Ruybalid <[log in to unmask]>
Reply To:
St. John's University Cerebral Palsy List
Date:
Thu, 27 Jan 2000 10:24:02 -0800
Content-Type:
text/plain
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This article   is interesting.
Mariana

Wednesday January 26 8:07 PM ET

Protein makes brain repair a no-go

By Merritt McKinney

NEW YORK, Jan 26 (Reuters Health) -- Scientists have identified a protein
believed to play a role in preventing the brain and
spinal cord from recovering from injury.

The discovery of the protein, called Nogo, may pave the way for better
treatment for brain and spinal cord injuries, strokes and
other diseases of the central nervous system, the author of one of three
reports on the topic told Reuters Health in an interview.

When a person has a brain or spinal cord injury, nerve cells called neurons
often survive, but axons, the long connections
between neurons, are clipped, according to Dr. Stephen M. Strittmatter, of
Yale University School of Medicine in New Haven,
Connecticut. Unlike axons in other parts of the body, those in the brain
and spinal cord -- the central nervous system -- do not
regenerate after they have been damaged, he explained.

Earlier research indicated that one or more molecules inhibited the
regrowth of axons, Strittmatter said. The identity of these
inhibitors was unknown, however, he noted.

But three teams of researchers, one led by Strittmatter, the others by Dr.
Frank S. Walsh at SmithKline Beecham

Pharmaceuticals in England, and Dr. Martin E. Schwab at the Brain Research
Institute in Zurich, Switzerland, have identified in
rats and humans a previously unknown gene that contains the blueprints for
Nogo -- a protein that inhibits the regeneration of
axons in the central nervous system. The three reports are published in the
January 27th issue of the journal Nature.

``Now there is a molecular target,'' Strittmatter said. A drug that blocks
Nogo might allow axons to regrow after an injury or
disease, Strittmatter explained in the interview. Besides helping people
with brain or spinal cord injuries, this type of drug might
also be useful in treating damage caused by stroke and the neurological
disease multiple sclerosis, he said.

But Strittmatter noted that Nogo may not be the only molecule that blocks
the regeneration of axons. ``This is one of the
inhibitors, but there's no proof that it's the only one,'' he said. ``Maybe
we need to block three or four at the same time to get a
good recovery.''

In an editorial that accompanies the reports, Drs. J.L. Goldberg and B.A.
Barres of Stanford University School of Medicine in
California, write that the discovery of Nogo ``is a landmark step on a long
road towards new treatments for patients suffering
from many neurological conditions, including spinal cord injury and stroke.''

However, the editorialists point out that encouraging the regeneration of
axons may not be enough to heal all injuries. Neurons
require stimulation throughout life in order to survive, but when the brain
or spinal cord is injured, sometimes this process is
interrupted, they note. Goldberg and Barres conclude that successful
treatment will probably depend on both blocking the
inhibition of axons as well as the stimulation of neuron growth. SOURCE:
Nature 2000;403:369-370, 383-384, 434-444.

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