For the first time American scientists have succeeded in reducing the symptoms of Parkinson's disease in apes. The research team led by Jefrey Kordower of the Rush-Presbyterian St. Luke's Medical Center in Chicago injected a virus that had previously been inserted with the genetic information for the formation of the protein GDNF into the brain of the monkeys. There, GDNF stimulated the growth of dopamine-producing neurons. These are greatly reduced in Parkinson's patients.

Until now, it has only been possible in rats to use viruses as a delivery vehicle to deliver genes for GDNF into the brain. Now, Kordower's team of genetically engineered viruses has succeeded in rhesus monkeys as well: Eight older age-related animals and 10 animals with parkinsonian-like symptoms produced by a venom received the gene for GDFN via virus injection into their nerve cells, One to two months after gene therapy, scientists were able to detect twice as much dopamine production in diseased brain sections as in untreated control animals. And not only that: 3 months after the treatment showed the monkeys in motor tests significantly better results than their non-treated conspecifics.

The cause of Parkinson's disease is the destruction of dopamine-producing neurons in the brain. A new formation of these nerve cells does not take place. The result: The communication between nerve cells via the messenger dopamine breaks down. Typical symptoms of the disease are tremor, muscle rigidity and motor disorders. Scientists discovered the GDNF protein in the early 1990s. It is produced in embryos in the brain stem and other tissues of the nervous system and promotes the growth of the nerve cells that make up the dopamine. Since then, options for the treatment of Parkinson's by GDFN are being investigated.

Despite the success in rats and in the rhesus monkeys closely related to humans, the scientists are still cautious. Before the therapy may be applied to humans, they want to rule out that GDNF in turn leads to a toxic shock in Parkinson's patients.

Ingo Ensminger and Science Ad


Recommended Editor'S Choice