By Don Finley

A drug already used in some leukemia patients prevented brain cells linked to Parkinson's disease from being destroyed in mice, a finding that could point to a way to slow progression of the disease, San Antonio researchers are reporting today.

The research is early, and the drug used in the experiment doesn't work well in the human brain. But similar drugs are in development that might better penetrate the brain as well as target the specific enzyme at fault more precisely, scientists said.

The researchers first discovered a mechanism at work in Parkinson's disease that prevents a protein called parkin from doing its job of keeping the brain clear of other proteins that can accumulate and kill off cells.

An enzyme linked to chronic myeloid leukemia blocks parkin from working, they found. When a leukemia drug was used in turn to block the enzyme — called tyrosine kinase c-Abl — it prevented destruction of those healthy cells.

The results were being published today in the Journal of Neuroscience.

About a half-million people suffer from the tell-tale tremors and stiffness of Parkinson's, which is caused by damage to the dopamine-producing cells in the brain.

“In Parkinson's disease, we know the number of patients is increasing,” said Syed Imam, the lead author of the paper and an adjunct assistant professor of medicine at the University of Texas Health Science Center. “The (current) treatments are mostly to improve symptoms. They do not address how to slow down the disease. Our studies were targeted at whether we could actually slow the progression.”

Imam, who joined the staff of the U.S. Food and Drug Administration after the research was completed, cautioned that the findings must still be duplicated in larger animals and then in people. But he said he was encouraged the same mechanism was confirmed in brain tissue taken from people who died of Parkinson's.

A mutation in the gene that produces parkin is known to cause an inherited form of Parkinson's disease that makes up less than 5 percent of total cases. Parkin was suspected in other cases, but the exact cause was unclear.

“They're showing that this molecule, c-Abl, when it is activated, it actually inactivates parkin and blocks its protective effects,” said Dr. Beth-Anne Sieber, a program director at the National Institute of Neurological Disorders and Stroke, which partly funded the research along with the Michael J. Fox Foundation, the San Antonio Area Foundation and others. “If you inhibit c-Abl activation, it lets parkin pursue its normal protective cell function.”

The drug — sold as Gleevec — doesn't penetrate the brain very well, and doesn't just block c-Abl. But it's been on the market for several years and is well studied, the researchers noted, while newer, more specific drugs are in the pipeline.

“We're excited about this because it does provide a specific mechanism in Parkinson's,” said Dr. Robert Clark, assistant vice president for clinical research at the health science center, and a co-author of the paper. “It's likely not the only mechanism. It's one of several different things going on in the course of Parkinson's. But it's exciting, too, because it's a pathway that can be targeted therapeutically.”