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Antidepressants May Slow Parkinson's

Study hints they block death of nerve cells

THURSDAY, Sept. 27, 2001 (HealthDayNews) -- Discovery of a hitherto unknown mechanism in Parkinson's disease raises the possibility that antidepressants might slow progression of brain-cell damage, researchers say.

Nerve cell death in Parkinson's can be caused by an excess release of dopamine, a protein essential for nerve function, say neuroscientists at the Boston University (BU) Medical Center. They say they have found a mechanism that creates damaging concentrations of dopamine, and that some widely used antidepressants can block that activity. The finding is reported in the Sept. 28 issue of Science.

"The identification of this mechanism is opening new pathways in terms of therapy," says lead researcher Isabelle Mintz, an assistant professor of pharmacology at BU.

Scientists know that dopamine is always being released from nerve cells. It is a neurotransmitter, a chemical that carries messages between those cells. The standard picture has dopamine being released from cell components called vesicles and then being taken up by proteins called transporters.

Working with animal tissue, Mintz's team found that under some circumstances, the transporter proteins reverse their activity, spilling out dopamine that attacks nerve cells in the substantia nigra, a region of the brain that controls movement. Some antidepressants are known to block transporter activity and thus might be effective in Parkinson's, Mintz says.

"The main one we are thinking of is bupropion, which currently is marketed as Wellbutrin," Mintz says.

But she says getting proof that bupropion will help Parkinson's patients will be a long-term process. "In order to establish a beneficial role, we need controlled clinical studies," Mintz says. The first step would be an animal test, probably using a primate. She says if that test is successful, "there is the possibility of going very quickly to clinical trials" in humans.

It is "an interesting suggestion," says Randy D. Blakely, director of the Center for Molecular Neurosciences at Vanderbilt University and author of an accompanying editorial that raises several possibilities other than the use of antidepressants.

"It is an interesting idea to go directly after the transporters with existing drugs, but that might not be the way to go," because many drugs that act on transporters are stimulants, including cocaine and amphetamines, Blakely says.

An indirect attack aimed at another neurotransmitter, glutamine, which is known to affect dopamine activity, might be more effective, Blakely says. A number of compounds that act on glutamine are being studied for use in seizure disorders, stroke and disorders of brain function, he says.

"In the laboratory, using experimental compounds, we could see if we can limit the export of dopamine and thus test the idea," Blakely says.

He says the major point is that the Boston researchers show that "dopamine can get out in a way that we hadn't thought too much about. Knowing that raises an interesting dimension of attack."

What To Do

While basic research continues, any impulse at self-medication for Parkinson's should be restrained. Bupropion is a potentially dangerous drug, and an overdose can cause hallucinations, seizures, chest pain, breathing difficulties and loss of consciousness.

Information about Parkinson's disease is available from the National Institute of Neurological Disorders and Stroke or the American Parkinson Disease Association.

SOURCES: Interviews with Isabelle M. Mintz, Ph.D., assistant professor of pharmacology, Boston University Medical Center, and Randy D. Blakely, director, Center for Molecular Neurosciences, Vanderbilt University, Nashville, Tenn.; Sept. 28, 2001, Science
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