X-Message-Number: 12316
Date: Tue, 24 Aug 1999 18:21:25 -0400
From: Jan Coetzee <>
Subject: Drug Takes New Approach To Stop Brain Damage

Drug Takes New Approach To Stop Brain Damage

By Maggie Fox, Health and Science Correspondent

WASHINGTON (Reuters) - A drug that blocks a gene responsible for
inflammation and cell
death could offer a new way to prevent brain damage resulting from
injuries or diseases such as
Alzheimer's, researchers said Tuesday.

The drug affects a protein known as COX-2, which is found throughout the
body and is
responsible for pain and inflammation. COX-2 is already targeted by a
new range of arthritis
drugs known as COX-2 inhibitors. But the new drug, developed by an
international team of
researchers, attacks the protein at the genetic level.

Dr. Nicolas Bazan and colleagues hope it might be used to prevent brain
damage from injuries,
Alzheimer's disease, stroke, Parkinson's and other conditions.

``One application of this knowledge that I dream of is in car
accidents,'' Bazan said in a
telephone interview.

``This can be sort of a first-line defense against brain damage and
brain death on the roadside,''
said the researcher, who was presenting his findings to a meeting of the
American Chemical
Society in New Orleans.

Drug companies have recently gambled that selectively blocking the COX-2
enzyme can reduce
pain without side effects, such as stomach bleeding, which aspirin and
related agents -- known
as non-steroidal anti-inflammatory drugs (NSAIDS) -- are notorious for.

But Bazan said COX-2 acts in a unique way in the brain, taking part in a
so-called cascade of
events that cause brain cells to die.

When one neuron is injured, as in a stroke or a blow to the head or even
in brain diseases, it can
send out chemical signals that affect nearby brain cells and cause them
to die, too. They die
over the hours and weeks after an injury.

Doctors are not sure why this happens, but many companies are working on
drugs that will cut
short this process.

The Argentine-born Bazan, working with colleagues at Louisiana State
University and the
Universidad de Alcala in Spain, said he found COX-2 was central to the

``We found the chemical signals within brain cells that turn on the
COX-2 gene,'' he said.

The two teams worked together to create a compound that would block this
signal. ``What this
will do is switch off the gene that encodes the protein COX-2,'' said
Bazan, who has applied for
a patent for the compound.

``We feel that this approach will be the way to develop a whole new
generation of COX-2
inhibitors,'' he said. ``We can really inhibit the consequences of

Bazan said that if ambulances carried his drug, it might be injected in
cases where the head was
injured, to prevent more neurons from dying. The window of opportunity
for preventing this cell
die-off is very narrow -- a few hours at most.

So far it has worked in human brain cells in laboratory dishes, as well
as in mice and rats,
Bazan said. He said the compound gets past the so-called blood-brain
barrier that keeps many
drugs from getting to brain cells, and seems to be harmless to the brain
cells themselves.

``It is also not toxic to the liver, kidney or stomach in animals,''
said Bazan, whose worked was
supported by the U.S. National Institutes of Health.

The only drug on the market to limit damage after a stroke is
Genentech's clotbuster Activase,
which is also known as tissue plasminogen activator or tPA, and it must
be given within three
hours to work.

But there are several other experimental drugs on the market that seek
to stop this damage even

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