Stevens, a recent recipient of a Mac Arthur Foundation “genius grant,” had found that other complement proteins in the immune system also played a role in brain development.
These results came from studying an experimental model of synaptic pruning in the mouse visual system.
The study has the potential to reinvigorate translational research on a debilitating disease.
Schizophrenia afflicts approximately 1 percent people worldwide and is characterized by hallucinations, emotional withdrawal and a decline in cognitive function.
They found that the C4 gene structure (DNA) could predict the C4 gene activity (RNA) in each person’s brain.
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They then used this information to infer C4 gene activity from genome data from 65,000 people with and without schizophrenia. People who had particular structural forms of the C4 gene showed higher expression of that gene and, in turn, had a higher risk of developing schizophrenia.
Unlike most genes, C4 has a high degree of structural variability.
Different people have different numbers of copies and different types of the gene.
The strongest signal by far was on chromosome 6, in a region of DNA long associated with infectious disease.
This caused some observers to suggest that schizophrenia might be triggered by an infectious agent.