A gene associated with schizophrenia plays a role in brain development and may help to explain the biological process of the disease, according to new Rutgers research.
In the study, published online in Biological Psychiatry, Bonnie Firestein, professor in the Department of Cell Biology and Neuroscience, says too much protein expressed by the NOS1AP gene, which has been associated with schizophrenia, causes abnormalities in brain structure and faulty connections between nerve cells that prevent them from communicating properly.
Firestein’s research indicates that an overabundance of a protein in the NOS1AP gene resulted in the dendrites — tree-like structures that allow cells to talk to each other and are essential to the functioning of the nervous system — being stunted in the developing brains of rats.
She and her colleagues found that too much of the NOS1AP protein in brain cells didn’t allow them to branch out and kept them deep within the neocortex, the portion of the brain responsible for higher functioning skills, such as spatial reasoning, conscious thought, motor commands, language development and sensory perception.
In the control group of rats in which NOS1AP chemical protein was not overexpressed, the cellular connections developed properly, with cells moving to the outer layers of the neocortex and enabling the nerve cells to communicate.
“When the brain develops, it sets up a system of the right type of connectivity to make sure that communication can occur,” says Firestein. “What we saw here was that the nerve cells didn’t move to the correct locations and didn’t have dendrites that branch out to make the connections that were needed.”
Although scientists can’t pinpoint for certain the exact cause of schizophrenia, they have determined that several genes, including NOS1AP, are associated with an increased risk for the disabling brain disorder and believe that when there is an imbalance of the chemical reactions in the brain, development can be disrupted.