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Research links 'ecstasy' to survival of key movement-related cells in brain

New research from the University of Cincinnati (UC) suggests that the widely abused club drug "ecstasy," or MDMA, can increase the survival of dopamine cells in the brain during fetal development.

Because these cells are critical in the regulation of voluntary movement, the findings, the researchers say, may lead to better therapies for neurological diseases like Parkinson's.

Led by Jack Lipton, PhD, professor of psychiatry, the study was presented today as an abstract at the Society for Neuroscience annual meeting in Atlanta.

"We're certainly not suggesting that this drug be used to treat diseases," said Lipton. "But finding new methods to enhance the survival of dopamine neurons is critical in developing new drugs for diseases such as Parkinson's.

"While MDMA itself isn't likely to be an appropriate therapy for neurodegenerative diseases, it may provide insights for developing new drugs that have similar properties.

"It's exciting to learn that an abused drug may have potential use for developing new therapeutics," he added. "It really makes you rethink your own preconceptions."

Dopamine is a neurotransmitter that has been found to regulate movement, balance, emotion and motivation, and it also affects pleasurable feelings in the brain. Researchers know that a loss of dopamine cells in the brain leads to the development of Parkinson's disease and possibly other movement disorders. Preventing dopamine cells from dying or aiding in the replacement of those cells is key to finding lasting therapies.

Lipton, director of the developmental neuroscience division in UC's psychiatry department, studies the long-term effects of abused drugs on the developing central nervous system. He noticed, during previous laboratory studies in rats, that prenatal exposure to MDMA increased growth of dopamine cells in the brain. His team then decided to study exposure to MDMA in cultured embryonic cells--where they confirme
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Source:University of Cincinnati


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