'Bad' gene causes schizophrenia
2007-05-03 06:45
Chicago - An international team of researchers said on Wednesday that they had conducted laboratory studies on mice that provide further evidence to show that a malfunctioning gene can cause both schizophrenia and depression.
The gene, DISC1, was first identified in 2000 in a large Scottish family with a history of multiple mental illnesses, but little is known about how the mutations in the gene interfere with biology to trigger mental disorders.
The hope is that having reproduced the defect in mice, those mice will serve as guinea pigs for future treatments for the disorders.
The investigators began their experiment by inducing mutations in a batch of mice using chemical compounds.
When they screened the mice they found they had two groups of mice with quite distinct mutations in the DISC1 gene.
Subsequent testing showed that one of the mutant mouse strains appeared to exhibit schizophrenia-type symptoms such as attention and memory deficits.
When those mice were treated with the antipsychotic drugs Haldol and Clozapine, the symptoms cleared up.
Similarly, tests on another batch of mice with a different mutation in the DISC1 gene suggested they were exhibiting symptoms of depression and when the rodents were treated with an antidepressant, Zyban, they also improved.
Professor David Porteous, chair of Human Molecular Genetics and Medicine at the University of Edinburgh, said the findings bolster previous research linking the gene with schizophrenia, depression and bipolar disorder.
Different types of damage to the gene
"We also found remarkable clear cut differences between the different types of damage to the gene and the treatment that was most effective. By analyzing how the brain changes and develops over time we would hope that this would lead to more effective drugs to treat such illnesses."
About one in 50 people worldwide will develop the symptoms of schizophrenia or bipolar disorder, otherwise known as manic depression, with the first signs often appearing in late adolescence or early adulthood.
Most cases arise in families with some sort of history of mental illness implying a strong influence of genes.
The study is published in the journal Neuron, and was a collaboration of researchers at Mount Sinai and the University of Edinburgh in Britain.