Pubdate: Mon, 01 Aug 2005
Source: News & Observer (Raleigh, NC)
Copyright: 2005 The News and Observer Publishing Company
Contact: https://miva.nando.com/contact-us/letter-editor.html
Website: http://www.news-observer.com/
Details: http://www.mapinc.org/media/304
Author: Paul Elias, AP Biotechnology Writer
Bookmark: http://www.mapinc.org/mdma.htm (Ecstasy)
Bookmark: http://www.mapinc.org/meth.htm (Methamphetamine)

PARKINSON'S-AFFLICTED MICE INJECTED WITH SPEED GOT BETTER

SAN FRANCISCO -- Illegal drugs such as Ecstasy and related amphetamines 
reversed the Parkinson's diseaselike muscle rigidity in mice, researchers 
reported Monday.

While cautioning such a surprising finding in mice doesn't translate 
directly to patients, the scientists said the research opens up new areas 
of exploration for an incurable brain disorder that afflicts 500,000 people 
in the United States.

"We hope that our study doesn't prompt all the Parkinsonians to go out to 
the street corners to deal for methamphetamine and Ecstasy," said Marc 
Caron, a Duke University Medical Center researcher in Durham, N.C., and 
co-author of the study.

Caron and his colleagues created mice through genetic engineering and drugs 
to be free of the brain chemical dopamine. Without dopamine, the rodents 
became rigid like Parkinson's patients.

The researchers then injected the mice with about 60 different chemical 
compounds, that are widely abused like Ecstasy and several others from the 
amphetamine family.

The mice receiving the speed showed dramatic results.

"These mice were frozen completely," said Duke researcher Raul Gainetdinov, 
another of the report's authors. "When we treated them and put them in 
water, they were able to swim."

The study is being published in the Public Library of Science's journal 
Biology, which is available free online. It was funded by a National 
Institutes of Health grant.

The paper suggests that amphetamines, especially when used with the one 
approved treatment that slows the effects of Parkinson's, helped make 
dopamine in the genetically engineered mice. Parkinson's patients lose 
brain cells that create dopamine, a chemical vital for motor function.

Investigating possible medicinal uses of such widely abused drugs like 
Ecstasy, an amphetamine derivative, is a highly contentious area of research.

Some research suggests that amphetamines - especially methamphetamine - 
damage brain cells when abused while other scientific reports are 
uncovering promising areas for therapeutic use of Ecstasy.

One high-profile paper published three years ago in the journal Science 
that showed Ecstasy killed dopamine-producing brain cells was later 
retracted when the researchers said they mistakenly used methamphetamine in 
their research.

Those results still showed methamphetamine to be toxic.

Caron said that amphetamine abuse is dangerous and unhealthy, but 
overshadows the possible medicinal benefits the drugs may have. Children 
have been given two forms of speed for years to combat attention deficit 
disorders while the brain naturally creates amphetaminelike chemicals, he said.

Meanwhile, two human experiments exploring Ecstasy's use as a psychotherapy 
drug to treat post-traumatic stress syndrome and terminal cancer patients 
are currently underway.

Parkinson's experts not affiliated with the Duke research team tempered 
their enthusiasm for a paper they found intriguing but incomplete.

Dr. William Langston, chief executive of the Sunnyvale-based Parkinson's 
Institute, said the paper could open up a new field of exploration in a 
so-far frustrating research area for scientists.

"The excitement is that they could be onto something quite novel," said 
Langston, who is also a board member of the Michael J. Fox Foundation for 
Parkinson's Research.

Still, he cautioned that the mice in the experiment didn't get the 
Parkinson's recognizable in people.

Others warned about reading too much into the research.

"There may be a more simple explanation than a dopamine-independent effect 
of amphetamines," said Dave Sulzer, a Parkinson's researcher at Columbia 
University Medical Center.

Sulzer said among other possible explanations not explored by the Duke team 
is that the amphetamines interfered with the drug used to block dopamine 
production in the mice.

He also noted that the researchers didn't test the amphetamines and 
dopamine inhibitors on naturally produced mice with normal dopamine levels 
for comparison's sake.

"It's a good paper," Sulzer said. "But it's really premature" to begin 
testing amphetamines on Parkinson's patients. Sulzer also noted that the 
amphetamines given to each mouse were excessively high.

"You would never give patients this amount," he said.
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MAP posted-by: Jay Bergstrom