Wed 5 Jul 2006(The Scotsman) - THE effects of Parkinson's disease
could be reversed by a drug which causes new brain cells to grow,
research suggests.
Scientists hope that the findings from the experimental drug could
lead to new treatments for patients with the debilitating disease.

There are currently no proven treatments to slow or halt the course
of Parkinson's disease, which affects 10,000 people in Scotland,
with drugs becoming less effective over time.

The progressive disease's symptoms of tremors, stiffness in the
limbs, slow movements and poor balance and co-ordination are caused
by the loss of neurons in the brain.

Now new tests in animals show that a drug, known as 7-OH-DPAT, which
mimics the effects of the nerve-signalling chemical dopamine, causes
new neurons to develop in the part of the brain where cells are lost
to the disease.

The team from the Mayo Clinic College of Medicine in Florida gave
the drug to rats with symptoms similar to Parkinson's in humans.

The rats were also given infusions of a fluorescent substance to
show how neurons in the brain were connecting. They were tested
before and after receiving the treatment to see how well they could
walk and move.

Animals treated with the drug had more than twice as many
multiplying cells as those who did not receive treatment.

Many of these new cells appeared to develop into mature neurons and
about 28 per cent appeared to be the key dopamine neurons. There was
also an 80 per cent improvement in movement and the rats' ability to
retrieve food by themselves after treatment.

The researchers, writing in The Journal of Neuroscience, said that
the effects appeared to last at least four months after treatment
ended.

Lead researcher Dr Christopher Eckman said: "There was a profound
behavioural effect of the treatment, even after it 'washed out' of
the system. This shows that the treatment affects the underlying
pathology."

The experimental animal drug is similar to others currently approved
to treat Parkinson's in humans.

Dr Eckman said while these were useful in treating the symptoms,
they had not been designed to prompt new neurons to grow.

He said that tweaking how these drugs work or developing new
compounds to boost neuron growth could provide an entirely new way
of treating Parkinson's.

Dr Eckman said this was the first study to show that the development
of new neurons from cells already in the brain could lead to better
movement in those treated.

The findings may also lead to new ways of treating other
degenerative diseases affecting the brain, such as Alzheimer's.

Many researchers are currently trying to find ways of replacing lost
neurons in Parkinson's disease.

One possible way that this could be achieved would be to transplant
new neurons grown from embryonic stem cells or other cells.

But this type of treatment is very difficult for technical reasons.
There is also some ethical concerns about the use of embryonic stem
cells, which are harvested from human embryos which are then
destroyed.

Dr Eckman said that a drug therapy would be much easier to give to
patients with Parkinson's.

The researchers are now looking at how different doses of existing
Parkinson's drugs affect the development of new cells. They hope to
then be able to test comparable doses in humans.

The National Institute of Neurological Disorders and Stroke in the
US described the research as "very exciting".

Dr Kieran Breen, the director of research at the Parkinson's Disease
Society in the UK, said: "The results of this study are interesting,
demonstrating this drug has a positive effect on both stem cells
within the brain and the growth of neurons and can lead to improved
movement in rats with Parkinson's.

"As the drug tested in the trial has similar effects to dopamine
agonists - a class of drugs currently used in Parkinson's treatment -
further studies are required to see if these currently available
treatments have a similar effect on stem cells within the brain and
the growth of neurons."

Dr Breen said the research helped further understanding of
Parkinson's.

LYNDSAY MOSS