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Schizophrenia Gene's Role May Be Broader, More Potent, than Thought
Date:11/19/2009

UCSF scientists studying nerve cells in fruit flies have uncovered a new function for a gene whose human equivalent may play a critical role in schizophrenia.

(Vocus) November 19, 2009 -- UCSF scientists studying nerve cells in fruit flies have uncovered a new function for a gene whose human equivalent may play a critical role in schizophrenia.

Scientists have known that the mutated form of the human gene – one of three consistently associated with schizophrenia – mildly disrupts the transmission of chemical signals between nerve cells in the brain.

The new study focuses on genes involved in “adaptive plasticity,” the capacity of nerve cells to compensate for a wide range of perturbations and continue to function normally.

Studies ranging from fruit flies to human have shown that if a nerve cell is functionally impaired then the surrounding cells can compensate and restore normal cell-to-cell communication. This type of “adaptive plasticity” stabilizes brain function, but the molecules involved remain largely unknown.

In the current study, the team screened 276 mutated, or disabled, fly genes to determine if their absence revealed a role in adaptive plasticity in the fruit fly nervous system. While absence of most of the genes had no impact on adaptive plasticity, the absence of the gene known as dysbindin did.

The finding, reported in the November 20, 2009 issue of Science, was dramatic, says the senior author of the study, Graeme Davis, PhD, Albert Bowers Endowed Professor and Chair of the Department of Biochemistry and Biophysics at UCSF.

“Mutation of the gene completely prevented the capacity of the neural c
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