Washington: Researchers led by Johns Hopkins claim to have identified the mechanisms rooted in two anatomical brain abnormalities that may explain the onset of schizophrenia and the reason symptoms don`t develop until young adulthood. Both types of anatomical glitches are influenced by a gene known as DISC1, whose mutant form was first identified in a Scottish family with a strong history of schizophrenia and related mental disorders. The findings could lead to new ways to treat, prevent or modify the disorder or its symptoms.
"Connections between neurons are constantly being made and broken throughout life, with a massive amount of broken connections, or ``pruning,`` happening in adolescence," Sawa says. "If this pruning doesn`t happen correctly, it may be one reason for the pathogenesis of schizophrenia," he adds. In the second study, published in the Feb. 25 issue of Neuron, Sawa``s team generated a new animal model of schizophrenia by temporarily shutting off the DISC1 gene in mice in the prefrontal cortex, a brain area known to differ in schizophrenic people. The new model allowed them to study other roles for DISC1 in the brain. The researchers created their novel model by, again, using RNA interference. They injected short pieces of the nucleic acid RNA engineered to shut off the DISC1 gene into cavities in the developing brains of mouse fetuses two weeks after conception. Tests showed that these snippets of RNA migrated into cells in the prefrontal cortex, part of the brain located near the forehead. This shutoff was temporary, with the gene`s function fully restored within three weeks, or about a couple of weeks after birth. At various times after the gene was reactivated, the scientists examined the animals`` brains and behavior, looking for differences from normal mice.
Sawa`s team found that in the DISC1 shutoff group, nerve cells in the prefrontal cortex that produce dopamine, one of the chemical signals that nerve cells use to communicate, were markedly immature as the animals entered adolescence. Furthermore, the animals showed signs of a deficit of interneurons, nerve cells that connect other neurons in neural pathways. They also found several behavioral differences between these mice compared to normal mice as the animals entered adolescence. Taken together, Sawa says, results of both studies suggest that these anatomical differences, which seem to be influenced by the DISC1 gene, cause problems that start before birth but surface only in young adulthood. ANI
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