When Toronto cancer researcher John Roder discovered his son Nathan had schizophrenia, he switched gears in his career, a change that has paid off with the discovery of a genetic link for the mental illness.

A cure for schizophrenia is likely years away, and will likely involve more than one factor, said Roder, a senior investigator at Toronto's Mount Sinai Hospital.

He estimated that schizophrenia research funding is about one-tenth the amount devoted to cancer, his first field of investigation after completing a PhD in immunology.

Switching so successfully from one field of basic science research to another is rare, but Roder's son was an inspiration.

"It's hard for people with mental illness to advocate for themselves," Roder told CBC Radio's Metro Morning on Thursday.

"If you imagine that Terry Fox had schizophrenia, probably he would have had that same grand idea, but he would never have got out of the first town because he would have been lost in his own thoughts."

Diagnosis brought 'fear and devastation and disbelief'

Roder said he spent about six months reading up on neuroscience and psychiatric disorders before making the switch when his son was diagnosed in his final year of high school in 2001.

Nathan Roder's grades started to slip, he stopped handing in assignments, and there was "a dramatic change in his ability to cope," his mother, Mary-Lou Roder, recalled.

"I remember seeing that word, schizophrenia, on the doors of the hospital, and it was like this fear and devastation and disbelief that this actually could have happened to us," she said.

While her husband changed his focus in hope of making a contribution to schizophrenia research, Mary Lou Roder became a caregiver for her son and an advocate for mental health who is trying to break the stigma surrounding the disease.

According to the Schizophrenia Society of Canada, about 300,000 Canadians, or one per cent of the population, will have the illness.

Response to treatment depends on mutation

As with Nathan, symptoms usually develop in late adolescence or early adulthood, and cases often occur in families with a history of mental illness.

As they report in Thursday's issue of the journal Neuron, Roder and colleagues in Toronto, Scotland and Japan used a mouse model to show that a malfunctioning gene can cause symptoms of schizophrenia and depression.

"These mice could represent a model system to explore novel treatment and preventative strategies for certain symptoms of major mental illness," the study's authors wrote.

Mutant mice carrying the malfunctioning gene, called Disrupted in Schizophrenia 1 or DISC1, showed the same kind of reduced brain volume seen in people with schizophrenia and depression, as well as similar biochemical abnormalities.

Mice with genes with one type of damage responded better to antipsychotics used to treat schizophrenia, while anti-depressants worked better in mice with another type of damage to the gene, the researchers found.

"We also found remarkable, clear-cut differences between the different types of damage to the gene and the treatment that was the most effective," said study co-author Prof. David Porteous of the University of Edinburgh.

An editorial accompanying the study cautions that mouse models offer a promising avenue of research for schizophrenia, which needs new strategies to reduce incidence and lessen severity. But the animal research is fraught with difficulties in interpretation and should be used cautiously, it warned.

"Psychiatric illnesses are highly prevalent, devastating to the affected individuals and their families, and enormously costly to society," wrote Nancy Low, of the department of psychiatry at Montreal's McGill University, and John Hardy, of the neurogenetics laboratory at the U.S. National Institutes of Health in Bethseda, Md.

John Roder said he talks to his son, now 21, about the work he is doing in the lab.   

"I'd say he feels very supported and cared for, and I think he appreciates the contributions that his dad has made," said Mary-Lou Roder.