Parkinson's - the missing clue
Australian researchers have found that certain cells in the cortex of the brain are missing in people with advanced Parkinson's not simply inactive as previously thought.
The researchers, led by Associate Professor Glenda Halliday at the Prince of Wales Medical Research Institute in Sydney, compared the brains of people who had suffered from Parkinson's disease with the brains of people who had died of other causes.
The discovery may lead to a deeper understanding of the causes of the disease.
"If we know the cause we can treat that instead of treating the symptoms," said Associate Professor Halliday.
Parkinson's disease affects about 50,000 Australians at any given time. It is most common in over-50s, but can affect those as young as five.
The disease affects affects two areas of the brain a part of the cortex, at the top of the brain, and an area of cells at the base of the brain that produce the neurotransmitter dopamine.
A neurotransmitter is a chemical that acts as a 'messenger' between nerve cells.
In a living person, a diagnosis of Parkinson's is given if two or more of the indicator symptoms are present tremor, stiffness of muscles, balance disturbance, and flow of muscles and if these are relieved by levadopa (a drug that mimics dopamine).
When a patient with Parkinson's undergoes a brain scan, the affected area of the cortex appears inactive.
It has been thought that this was because the cells were no longer working, and that the inactivity was a result of the loss of dopamine production in the lower part of the brain.
But it turns out they are actually missing, with 80 per cent of the area disappearing over the first 10 years of the disease.
The area of brain lost is about the size of the fingernail on the little finger.
The particular cells in the cortex are those that go down into the spinal cord and activate the nerve cells that control the muscles.
"If you get deficits in those regions of the cortex, then that must be influencing the difficulties the patients are having," said Associate Professor Halliday.
The discovery of the loss of cells explains why treating Parkinson's with levadopa is only effective for about five years.
"Previously, everyone has been trying to treat the cells as if they are active," said Associate Professor Halliday.
"So now we can think of other types of treatment, instead of treating cells that don't exist."
One option might be to try to stimulate other areas of the cortex to take over the role of the lost area before the cells die out.
The problem would be identifying patients at risk before the onset of symptoms, because once symptoms have begun it would be too late to begin 'retraining'.
The next phase for the researchers will be to try and figure out what is causing the death of the cells in the cortex, said Associate Professor Halliday.
"If we can look more in the cortex and see what is causing the degeneration, then we might be able to find out what's causing the disease."
The research was made possible by a brain donor program run by the Prince of Wales Medical Institute for the past 15 years. The 'brain bank' includes those donated by people with neuro-degenerative diseases, but also those without such diseases to serve as a comparison.
The study is expected to be published later this year.