New Brunswick, NJ, December 1, 2014 – According to Genetic Engineering & Biotechnology News, “Researchers at Rutgers report that a gene associated with schizophrenia plays a role in brain development and may help to explain the biological process of the disease. The team published its study (“NOS1AP, a protein implicated in schizophrenia, controls radial migration of cortical neurons”) in Biological Psychiatry. Bonnie Firestein, Ph.D., 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.”
Dr. Firestein’s research indicates that an overabundance of a protein in the NOS1AP gene resulted in the dendrites 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.
“When the brain develops, it sets up a system of the right type of connectivity to make sure that communication can occur,” says Dr. 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.”
“Our studies show for the first time a critical role for the schizophrenia-associated gene NOS1AP in cortical patterning, which may contribute to underlying pathophysiology seen in schizophrenia.”
“The next step would be to let the disease develop in the laboratory and try to treat the over expression of the protein with an antipsychotic therapy to see if it works,” explains Dr. Firestein.
For the complete article, click here.
Dr. Firestein’s research indicates that an overabundance of a protein in the NOS1AP gene resulted in the dendrites 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.
“When the brain develops, it sets up a system of the right type of connectivity to make sure that communication can occur,” says Dr. 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.”
“Our studies show for the first time a critical role for the schizophrenia-associated gene NOS1AP in cortical patterning, which may contribute to underlying pathophysiology seen in schizophrenia.”
“The next step would be to let the disease develop in the laboratory and try to treat the over expression of the protein with an antipsychotic therapy to see if it works,” explains Dr. Firestein.
For the complete article, click here.
