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Gene Mutations Before and After Birth Make a Difference in Diagnosis

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(Great Neck, N.Y. - January 11, 2010) — Johns Hopkins researchers have uncovered new findings that suggest that manipulations of the DISC1 gene during prenatal periods, postnatal periods or both may have different effects in mice. These changes could lead to separate types of brain alterations and behaviors with resemblance to schizophrenia or mood disorders. The findings, reported online Jan. 5 in Molecular Psychiatry, could eventually help researchers treat mental illness in people or even prevent it.

"Right now," said lead author Associate Professor Mikhail Pletnikov, M.D., Ph.D., "we cannot treat or reverse all the abnormalities associated with schizophrenia or major mood disorders, but our research gives us hope that we can eventually target some of these abnormalities that are currently considered incurable. If we catch these problems early enough, we may someday be able to prevent schizophrenia or depression from developing."

The Method

Scientists have long eyed mutations in a gene known as DISC1 as a possible contributor to schizophrenia and mood disorders, including depression and bipolar disorder. To manipulate DISC1 expression during different periods, the researchers crafted a novel mouse model in which a mutant form of the gene could be turned off by feeding the animals small amounts of the antibiotic doxycycline in their chow.

Using this model, Pletnikov's team generated four groups of mice: those that expressed mutant DISC1 prenatally (Pre), those that expressed mutant DISC1 postnatally (Post), those that expressed it during both periods (Pre+Post), and those that never expressed it (NO).

When the mice were about two-months-old, the researchers put the animals through a battery of behavioral tests designed to measure characteristics similar to schizophrenia and depression in humans, such as abnormal social interactions and heightened aggression under stress, comparing these animals with "control" animals that didn't express the mutant gene.

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