For the first time, researchers have found evidence that Parkinson's disease might spread to healthy nerve cells implanted into a patient's brain.

In postmortem studies, researchers found that a small minority of implanted cells in three patients had acquired traits associated with the disease. But for five other transplant recipients, the implanted neurons appeared healthy and functioning at the time of death, up to 16 years after surgery.

The finding could have implications for the use of stem cells to treat Parkinson's. These proposed therapies would implant healthy nerve cells into a patient's brain to replace cells damaged by the disease and partially relieve symptoms, mainly the poor control of body movement characteristic of Parkinson's. Doctors would derive new nerve cells from embryonic-like stem cells, rather than taking nerve cells from human fetuses, as was done for the patients in the new studies.

Healthy survival of most of the implanted neurons bodes well for the stem cell approach, comments stem cell–therapy researcher Viviane Tabar of the Memorial Sloan-Kettering Cancer Center in New York City. But scientists need to understand why some cells unexpectedly developed Parkinson's-like conditions, she says.

"This goes to prove how little we understand Parkinson's disease," Tabar says. "I'm not closing my lab and giving up on stem cell therapies for Parkinson's. It's just an opportunity to learn more about how to do these therapies correctly."

In a trio of studies published online April 6 in Nature Medicine, scientists in Sweden, England, Canada and the United States searched the brains of the transplant recipients for cells that contained clumps of the protein alpha-synuclein. The occurrence of such clumps in nerve cells is often characteristic of Parkinson's.

In the three affected patients, only 2 to 5 percent of the implanted nerve cells contained these protein clumps, says the lead researcher on one of the studies, Patrik Brundin of the Wallenberg Neuroscience Center at Lund University in Sweden. "That would suggest that it could take several decades before the majority of cells had [protein clumps] in the transplant," Brundin says.

It remains unclear why some transplanted cells developed clumps, the researchers say. The presence of alpha-synuclein in areas of the diseased brain near the transplant could have induced the creation of more of the protein in a kind of chain reaction, Brundin suggests.

Other factors could also explain the appearance of the protein, comments Curt Freed, a neuroscientist at the University of Colorado in Denver who has performed 61 fetal nerve cell transplants on Parkinson's patients but was not involved in the current studies. For example, stress on the cells during transplantation could also cause them to go awry in ways that produce the protein, Freed says.

The link between the protein clumps and Parkinson's is still debated, Freed notes, because alpha-synuclein is sometimes seen in nerve cells of people who do not have the disease.

"It just shows how complicated these [transplant] procedures are," says Rudolph Jaenisch, a stem cell researcher at the Whitehead Institute for Biomedical Research in Cambridge, Mass. "But it doesn't mean that they're useless."

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