A drug has been identified as a possible protector from Parkinson’s disease, according to a new study.

A drug more commonly dished out to transplant patients may be a good way at protecting brain cells from “rogue” genes which can lead to Parkinson’s disease, it is said.

Alex Whitworth and the team, based at the University of Sheffield, said that while rapamycin is no “wonder drug” for the treatment of the condition, the study proves that animal and human models that were used may be particularly valuable in discovering new drugs for directly treating the condition.

Dr Kieran Breen, who funded the work in his capacity as the director of research and development at the Parkinson’s Disease Society (PDS), explained: “It’s early days yet, and there’s a great deal of work to be done before we will know if these findings can be applied to all forms of Parkinson’s.

“But the discovery of this pathway may be the key to developing new drugs that could slow or even stop the progressive loss of nerve cells in the brain.”

In its capacity as a charitable force, the PDS announced last week that it is to donate £380,000 to the University of Edinburgh to understand the role of nerve cells in the progression of the condition.

Approval has been given for the world's smallest, longest-lasting rechargeable Deep Brain Stimulator (DBS) for Parkinson's Disease. Deep Brain Stimulation (DBS) involves the use in Parkinson's Disease of electrodes that are implanted into the brain and connected to a small electrical device that can be externally programmed. For more information go to Deep brain stimulation. The new small device is called the Brio neurostimulator. It is very thin and light, and only slightly bigger than a man's wrist watch. Additionally, the device has the greatest recommended implant depth of any rechargeable DBS device. The thin profile and greater implant depth potentially makes the neurostimulator less noticeable and more comfortable for patients. The Brio DBS system delivers mild electrical pulses to specific targets in the brain, stimulating the structures that are involved in muscular movement. The system consists of a neurostimulator – a surgically implanted battery-operated device that generates the electrical pulses – and leads which carry the pulses to the brain to influence the irregular nerve signals responsible for the symptoms of Parkinson’s Disease.

A pair of genes transplanted into the brains of lab rats can lead to the production of a neurochemical that is in short supply in many people with Parkinson's disease.

But what happens if the irrevocable delivery of the genes goes bad and causes unwanted side effects?

That concern has been on the minds of researchers seeking ways to spur brain cells into producing the neurochemical, dopamine.

Scientists at the University of Florida say they may have an answer for transplanted genes that may have run amok.

In an article published in the online version of the journal Molecular Therapy, a team at UF's McKnight Brain Institute and Powell Gene Therapy Center report that a common antibiotic appears to be able to slow down or turn off the genes after they have been transplanted.

This could be significant, because the UF researchers think earlier experimental attempts using growth factors - naturally occurring substances that cause cells to grow and divide - to revive dying brain cells and get them to produce dopamine again may have failed because they occurred too late in the course of the disease.

Doctors would be reluctant to try the gene transplant technique for revitalizing dopamine production if it carried the risk of inflicting permanent negative side effects on people who are still relatively health because their Parkinson's disease is in early stages.

Ronald Mandel, a professor of neuroscience at UF, and his colleagues have been studying the use of a virus as a "vector" that delivers the genes needed to protect brain cells that produce dopamine.

"We have worked every day for 10 years to design a construct to the gene delivery vector that enhances the safety profile of gene transfer for Parkinson's disease," Mandel says.

In the technique the UF team has been exploring, the two transplanted genes must work together to produce the protein molecule that plays a key role in the process.

The researchers have now discovered that the antibiotic doxycycline, depending on the dose given, can slow down or turn off that protein production by the transplanted genes.

"With that added measure of safety, we believe we can intervene with gene transfer in patients at earlier stages of the disease," Mandel says.

Doxycycline, a member of the tetracycline class of antibiotics, is used to treat various forms of bacterial infection and acne.

If the UF researchers are right, this could be the first time scientists would be able to regulate a gene therapy after the treatment has been delivered.

"With this technique, you could adjust the therapy in the patient," said Fredric P. Manfredsson, a postdoctoral associate in UF's department of neuroscience. "That would be extremely helpful because no one is really certain yet what dosage is required for a protective effect in humans."

Being able to control gene regulation could help the development of safety gene therapies, according to Mark Tuszynski, a professor of neurosciences and director of the Center for Neural Repair at the University of California, San Diego.

"The work of Dr. Mandel and colleagues brings us an important step closer to this goal," says Tuszynski, who had no involvement in the UF research