Do you have an axe to sell? What is with all your posts on pseudonutrition?

Bill

Hmmmmmm ......

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Source: Johns Hopkins Medical Institutions     Released: Mon
03-Jan-2005, 11:50 ET
Embargo expired: Wed 05-Jan-2005, 13:00 ET
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Antibiotics Protect Nerves in Mice by Turning on Genes
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LOU GEHRIG'S DISEASE PENICILLIN ALS GLUTAMATE CEFTRIAXONE ANTIBIOTICS
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Description

A family of antibiotics that includes penicillin may help prevent nerve
damage and death in a wide variety of neurological diseases, including
Lou Gehrig's disease, dementia, stroke, and epilepsy, Johns Hopkins
researchers have found.

Newswise  A family of antibiotics that includes penicillin may help
prevent nerve damage and death in a wide variety of neurological
diseases, including Lou Gehrig's disease, dementia, stroke, and
epilepsy, Johns Hopkins researchers have found.

The antibiotics' beneficial effects, discovered in experiments in the
lab and with mice, are unrelated to their ability to kill bacteria, the
researchers report in the Jan. 6 issue of Nature. Instead, the drugs
squelch the dangerous side of a brain chemical called glutamate by
turning on at least one gene, thereby increasing the number of
"highways," or transporters, that remove glutamate from nerves.

"It would be extremely premature for patients to ask for or take
antibiotics on their own," says the study's leader, Jeffrey Rothstein,
M.D., Ph.D., director of the Robert Packard Center for ALS Research at
Johns Hopkins and a professor of neurology and of neuroscience. "Only a
clinical trial can prove whether one of these antibiotics can help and
is safe if taken for a long time."

In mice engineered to develop the equivalent of Lou Gehrig's disease,
daily injections of an antibiotic called ceftriaxone, started just as
symptoms tend to surface, delayed both nerve damage and symptoms and
extended survival by 10 days compared to untreated animals. Lou
Gehrig's disease, or amyotrophic lateral sclerosis (ALS), in people
causes progressive weakness and paralysis and ends in death, usually
within three to five years of diagnosis.

"We're very excited by these drugs' abilities," says Rothstein. "They
show for the first time that drugs, not just genetic engineering, can
increase numbers of specific transporters in brain cells. Because we
study ALS, we tested the drugs in a mouse model of that disease, but
this is much bigger than ALS. This approach has potential applications
in numerous neurologic and psychiatric conditions that arise from
abnormal control of glutamate."

A large, multi-center clinical trial planned for the spring will help
determine the best dose of and schedule for ceftriaxone in people with
ALS, and will measure whether the known risks of long-term antibiotic
treatment are worth it, he says. The drug is currently approved by the
U.S. Food and Drug Administration and used to treat bacterial
infections in the brain.

More than a dozen of penicillin's relatives, known as beta-lactam
antibiotics, were among protective agents identified by a National
Institutes of Health-funded project to screen 1,040 Food and Drug
Administration-approved drugs for new uses. The newfound ability of
these antibiotics to activate glutamate transporters and to protect
nerves, and the drugs' potential therapeutic use in neurological
conditions, are covered by patent applications held by Rothstein and
Johns Hopkins and licensed to Ruxton Pharmaceuticals Inc.

Of the antibiotics, penicillin protected nerve cells best in laboratory
dishes, but ceftriaxone had the best results in mice, probably because
it more easily crosses into the brain from the blood, the researchers
report.

Rothstein and his colleagues determined that the antibiotics' benefit
stems from their newly recognized effect on glutamate's Jekyll-and-Hyde
effects. In the brain, glutamate normally excites nerves so that
electrical signals can travel from one to the next. But too much of the
chemical can overstimulate and kill nerves, a factor in ALS and some
other diseases.

In a series of experiments, the researchers discovered that the
antibiotics activate the gene encoding glutamate's main transporter in
brain cells. Rats and mice that received daily ceftriaxone for up to a
week had triple the usual amount of the transporter, known as GLT1, in
their brain cells, an effect that lasted for up to three months after
treatment.

"Glutamate is just one of many messengers brain cells use to
communicate with one another, and this is just one of the transporters
that move glutamate," says Rothstein. "So if you can find the right
drug, you might be able to specifically affect other transporters,
too."

Because ceftriaxone only protects against glutamate damage, just one
problem in ALS, it's not surprising that the mice eventually succumbed
to weakness and paralysis despite treatment, he says.

"If we can find drugs that protect against other causes of nerve death
in ALS, the combination might offer a real therapy, much like using
drug combinations to treat cancer," says Rothstein. "The more we know
about ALS and other neurological diseases, the better our chances of
finding ways to prevent nerve death by all causes."

The research was funded by the National Institute of Neurological
Disorders and Stroke, the Muscular Dystrophy Association and the Robert
Packard Center for ALS Research at Johns Hopkins. The ALS mice were
provided by Project ALS.

Authors of the paper are Rothstein, Sarubhai Patel, Melissa Regan,
Christine Haenggeli, Yanhua Huang, Dwight Bergles, Lin Jin, Margaret
Dykes Hoberg, Svetlana Vidensky, Dorothy Chung and Shuy Vang Toan, all
of Johns Hopkins; Lucie Bruijn of The ALS Association; and Zao-zhong
Su, Pankaj Gupta and Paul Fisher of Columbia University Medical Center.

---
Under a licensing agreement between Ruxton Pharmaceuticals Inc. and The
Johns Hopkins University, Rothstein is entitled to a share of royalty
received by the University on sales of products described in this
study. Rothstein and the University own Ruxton Pharmaceuticals Inc.
stock, which is subject to certain restrictions under University
policy. Rothstein is a paid consultant to Ruxton Pharmaceuticals Inc.
The terms of these arrangements are being managed by The Johns Hopkins
University in accordance with its conflict of interest policies.

On the Web:
http://www.nature.com/nature

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2005 Newswise.  All Rights Reserved.

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Tom

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