MDMA "Miracle Cure" for Parkinsons?

Dana Beal dana at phantom.com
Wed Aug 10 11:12:58 EDT 2005


From: writch at writch.com
Subject: MAPS: new studies show MDMA to be effective in treating 
parkinsons

Some of you might have heard me mentioning this a few years back.   
I've seen anecdotal studies which indicated that MDMA (Ecstasy) was 
amazing in restoration of lost functionality in Parkinson's.  In 
particular heard about a gymnast who was able to do backflips again 
after taking some.

If you think about it, it's really pretty funny.  The 'miracle cure' 
for Parkinson's due to successful attempts at evasion of drug law 
restrictions (If you recall, they had to change the drug laws to deal 
with Ecstasy and those things like it).

There are some clinicals, too (below and linked), for those of you who 
would prefer numbers to stories:

p.s., you might sign up for the MAPS forum yourself (see the bottom of 
the message for the link).

Begin forwarded message:

From: "Nikki"
Date: August 8, 2005 3:35:30 PM MDT
To: <MAPS_forum at maps.org>
Cc: Subject: MAPS: new studies show MDMA to be effective in treating 
parkinsons

August  2, 2005.  Ironically, after NIDA-funded researchers Drs. McCann 
and Ricaurte claimed that MDMA damaged dopamine neurons and could cause 
Parkinson's disease, a claim that they later had to retract, new 
research ( http://u.pvnm.org/-l-x_n-I_c ) conducted at Duke University 
Medical Center has shown that MDMA is the most effective of 60 drugs 
tested in reversing the symptoms of Parkinson's disease! This research 
was discussed in an article in News-Medical.Net.

http://u.pvnm.org/-l-x_n-J-J

From: News-Medical.net

Durham, N.C. --

  Amphetamines, including the drug popularly known as Ecstasy, can 
reverse the symptoms of Parkinson's disease in mice with an acute form 
of the condition, according to new research at Duke University Medical 
Center.

  The researchers caution that the findings in animals do not suggest 
Parkinson's disease patients should find relief by taking amphetamines, 
which are drugs of abuse with many dangerous side effects. The findings 
rather indicate that drugs with similar chemical attributes might offer 
useful alternatives to current therapies, the researchers said.

  The new study also shows that amphetamines -- normally thought to act 
by increasing dopamine concentrations in the brain -- correct the 
behavioral abnormalities associated with Parkinson's in mice devoid of 
the brain messenger. Dopamine normally acts on dopamine receptors -- 
protein switches on the surface of neurons -- to stimulate brain 
processes that affect movement, emotion, pleasure and mood.

  Parkinson's disease stems from the degeneration of neurons in a brain 
region that controls movement. That degeneration, in turn, leads to a 
shortage of the chemical messenger dopamine. The finding that 
amphetamines can alter movement independently of dopamine opens up new 
directions in the search for prospective anti-Parkinsonian drugs, the 
researchers said.

  The researchers, led by James B. Duke professor of cell biology Marc 
Caron, Ph.D. and Assistant Research Professor Raul Gainetdinov, M.D., 
Ph.D., of Duke, made the discovery after testing the utility of more 
than 60 compounds for reversing Parkinson's symptoms in a mouse model 
of the disease. Developed by the Duke team, the mice lack detectable 
brain levels of dopamine and experience essentially all the symptoms of 
Parkinson's disease for several hours before recovering their normal 
behavior. Caron is also a researcher of the Duke Institute for Genome 
Sciences & Policy.

  The team reports its findings in the August 2005 issue of Public 
Library of Science (PLoS) Biology. The research was sponsored by the 
National Institutes of Health and a donation from The Long Island 
Community Foundation, a division of The New York Community Trust.

  "This model is exciting because it allows us to examine the potential 
contribution of systems other than dopamine to Parkinson's disease," 
said Caron. "We may be able to discover avenues for treatment that had 
never been thought about before or that were impossible to 
investigate."

  The new mouse model enables the researchers to acutely eliminate 
dopamine, exposing systems contributing to the disease that may not 
have been obvious before, he explained. The severity of disease 
symptoms in the mice also provides a very sensitive test for compounds 
with potential therapeutic value, the researchers said.

  In the United States, at least 500,000 people suffer from Parkinson's 
disease, and about 50,000 new cases are reported annually, according to 
the National Institute of Neurological Disorders and Stroke. These 
figures are expected to rise as the average age of the population 
increases. Symptoms of the disease include tremors, slow movement or an 
inability to move, rigid limbs and a shuffling gait. Progression of the 
disease also leads to severe impairment in cognitive function.

  Dopamine replacement therapy which involves administration of the 
dopamine precursor, L-DOPA, remains the gold standard for Parkinson's 
treatment, said Tatyana Sotnikova, Ph.D., of Duke. However, the 
efficacy of the therapy wanes with time, and patients often develop 
fluctuations in motor performance and other adverse reactions.

  In the current study, the researchers treated mice unable to recycle 
dopamine with a drug that also prevented them from manufacturing the 
brain messenger. The brains of the mice therefore lack detectable 
levels of dopamine and the animals exhibit all the symptoms of 
Parkinson's disease for up to 16 hours. Those symptoms included 
severely impaired movement, rigidity and tremor. When treated with 
L-DOPA, the symptoms disappeared as the animals resumed normal 
movement.

  Surprisingly, the researchers reported, treating mice lacking dopamine 
with high doses of amphetamine derivatives including methamphetamine 
and MDMA, otherwise known as Ecstasy reversed those symptoms. Ecstasy 
was most effective at counteracting the manifestations of Parkinson's 
symptoms in the mice, with the beneficial effects becoming more 
pronounced with increasing dose.

  The researchers also report that low doses of amphetamines could, when 
combined with L-DOPA, potentiate minimally effective doses of L-DOPA in 
the mice. This could have important considerations in reducing some of 
the side effects of current therapy.

  "The locomotor stimulating effect of amphetamine and its derivatives 
are classically thought to result from a massive flood of dopamine," 
said Sotnikova. "However, the mice have only a tiny fraction of 
dopamine, which cannot be recycled, precluding a rise in dopamine as 
the possible mechanism.

  "Taken together, the findings indicate that Ecstasy can improve 
movement control independently of dopamine and, most importantly 
provide evidence that drug activation of other neuronal pathways may be 
sufficient to restore movement even in the virtual absence of dopamine 
neurotransmission," she added.

  Amphetamines might reverse the animal's symptoms through their effects 
on a different group of receptors called trace amine receptors, the 
researchers suggested. Recent evidence showed that amphetamines act on 
trace amine receptors in addition to dopamine transmission, yet little 
is known about their physiological role in mammals.

  The current findings are particularly promising given the severity of 
symptoms in the mice completely lacking dopamine, said Gainetdinov. "We 
think that this new animal model provides a much more stringent test 
for potential drugs that might prove efficacious in patients with 
Parkinson's disease."

  Many of the previously developed animal models of Parkinson's disease 
have reduced, but detectable, levels of dopamine and do not show all 
the characteristics of Parkinson's disease, making studies of potential 
therapeutic methods in those animals less clear, Gainetdinov said. On 
the other hand, animals permanently lacking dopamine cannot survive, he 
added.

  While the results are promising, the researchers cautioned, Ecstasy's 
ability to stimulate movement in the mice occurred only with high doses 
of the drug. Such high doses might destroy nerve tissue in normal mice 
and in humans, who are generally more sensitive than mice to such 
drugs.

  "Amphetamines are controversial drugs, and there's no reason to 
suggest that amphetamines themselves should be used to treat 
Parkinson's," Gainetdinov said. "However, the chemical structure of 
amphetamines may lead to new, amphetamine-like drugs, that might 
provide a more lasting and beneficial alternative to L-DOPA in the 
treatment of Parkinson's disease."

  Collaborators on the study include Jean-Martin Beaulieu, Larry S. 
Barak and William C. Wetsel all of Duke.
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