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Home | Pregnancy Timeline | News Alerts |News Archive Dec 4, 2014

 

 






 

 

Excess protein may trigger schizophrenia

Rutgers University scientists observed during research that too much protein produced by the NOS1AP gene causes brain abnormalities and faulty neural connections.

The NOS1AP gene may be associated with schizophrenia, but it also plays a key role in normal brain development, a discovery that may help explain the biological process of schizophrenia. In the study published in Biological Psychiatry, Bonnie Firestein PhD, professor in the Department of Cell Biology and Neuroscience at Rutgers University, states that too much of the NOS1AP protein made by the NOS1AP gene, causes abnormalities in dendrite formation. This leads to faulty connection between nerve cells and limited signal exchange.


Dr. Firestein's research indicates that an overabundance of the NOS1AP protein produced by the NOS1AP gene resulted in dendrites being stunted in the developing brains of rats. Dendrites are the tree-like, branching structures which allow cells to transfer electrical stimuli between each other. This data transfer is essential to the function of the nervous system.


Dendrites are kept deep within the neocortex the portion of the brain responsible for spatial reasoning, conscious thought, motor commands, language development and sensory perception. However, in the rat control group in which the NOS1AP protein was kept at normal levels, dendrites developed properly, branching to the outer layers of the neocortex and enabling intracellular communication.


"As the brain develops, it sets up a system of connectivity that makes sure communication can occur. We observed that if nerve cells didn't move to their correct location, they didn't produce dendrites that can branch out and make necessary connections."

Bonnie Firestein, professor, Department of Cell Biology and Neuroscience, Rutgers University, New Jersey, USA


Although scientists as yet cannot pinpoint the exact molecular relationships which give rise to schizophrenia, they have determined several genes, including NOS1AP, associated with an increase in risk for the disabling brain disorder.

Firestein has been working with Rutgers geneticist Linda Brzustowicz, professor and chair of the Department of Genetics, and co-author on the paper who first began investigating the genetic link between NOS1AP and schizophrenia a decade ago. While about 1 percent of the general population suffers from schizophrenia, the risk increases to about 10 percent in first degree relatives of an individual with the disease. In some families with multiple individuals affected with schizophrenia, NOS1AP has been identified as a contributing factor.


Since the prefrontal cortex — that part of the brain associated with schizophrenia — matures throughout adulthood, Firestein believes it is possible that drug treatments could be targeted to the disease in adolescents when symptoms first appear.


"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 anti-psychotic therapy to see if it works," adds Firestein.

Abstract
Background
Where a neuron is positioned in the brain during development determines neuronal circuitry and information processing needed for normal brain function. When aberrations in this process occur, cognitive disorders may result. Patients diagnosed with schizophrenia have been reported to show altered neuronal connectivity and heterotopias. To elucidate pathways by which this process occurs and become aberrant, we have chosen to study the long isoform of nitric oxide synthase 1 adaptor protein (NOS1AP), a protein encoded by a susceptibility gene for schizophrenia.

Methods
To determine whether NOS1AP plays a role in cortical patterning, we knocked down or co-overexpressed NOS1AP and a GFP or TagRFP reporter in neuronal progenitor cells of the embryonic rat neocortex using in utero electroporation. We analyzed sections of cortex (ventricular zone VZ, intermediate zone IZ, and cortical plate CP) containing GFP or TagRFP positive cells and counted the percentage of positive cells that migrated to each region from at least three rats for each condition.

Results
NOS1AP overexpression disrupts neuronal migration, resulting in increased cells in IZ and less cells in CP, and decreases dendritogenesis. Knock down results in increased migration, with more cells reaching the CP. The phosphotyrosine binding region, but not the PDZ-binding motif, is necessary for NOS1AP function. Amino acids 181-307, which are sufficient for NOS1AP-mediated decreases in dendrite number, have no effect on migration.

Conclusions
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.

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