Yifu Deng of QUT's School of Public Health studied the interplay between genetics, smoking and the development of Parkinson's disease with 400 people who had Parkinson's disease and 400 people without it.

Dr Deng looked at the genetic background of individuals in each group for the presence of the CYP2D6 gene, which had previously been suggested to metabolise the chemical compounds found in cigarette smoke, in both groups.

He found that smokers with the gene who metabolised the cigarette smoke compounds quickly were less likely to be protected than those who metabolised the chemical compounds more slowly.

"It seems that if the chemical compounds stay in the body longer they are more likely to have a preventative effect," Dr Deng said.

"It also seems that if you have the gene but you are not a smoker the gene may have no use in preventing Parkinson's."

Dr Deng said it was not known how the cigarette smoke compounds protected against Parkinson's.

He warned that there were still many smokers who suffered from Parkinson's. Additionally, smoking was notorious for causing cancers.

Parkinson's disease is a common degenerative neurological disease in the elderly, affecting up to 4.9 percent Australians aged 55 and over.

"Our study findings aid in further understanding of the causes of Parkinson's disease and may help identify people who are at higher risk of the disease," he said.

The study is the first to look at the genetic epidemiology of Parkinson's disease by addressing individual genetic types in relation to cigarette smoke metabolism.

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For the study, Hare and colleagues first examined whether CNTF receptors were present and functional in the heart muscles by staining heart muscle cells with a chemical that would highlight the receptors when viewed under a high-powered microscope. These tests showed that CNTF receptors were located on the cells' surfaces.

Next, they randomly assigned a set of leptin-deficient mice into three groups: a third received daily abdominal injections of CNTF, a third were fed a calorie-restricted diet, and a third ate as much as they wanted. The researchers used the same three approaches plus leptin supplements on another group of leptin-resistant mice.

Ultrasound exams of the hearts after four weeks showed that CNTF decreased the thickness of the wall dividing the heart chambers by as much as 27 percent, decreased the thickness of the wall at the back of the heart by as much as 29 percent and overall volume of the left ventricle by as much as 41 percent. As expected, leptin supplements did not change left ventricular wall thickness.

CNTF-treated mice also showed reduced heart-cell width, a direct measure of the amount of hypertrophy.

More research is to be done before CNTF can be used to treat patients, Hare says, as people can develop antibodies to CNTF. The scientists next plan to test CNTF in other animal models of hypertrophy not related to obesity.

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