Genetic Causes of Schizophrenia Update

It’s exciting to report that we are significantly closer to understanding what causes schizophrenia. More than two million Americans are diagnosed with schizophrenia, which is characterized by delusional thinking, hallucinations, and speech and behavioral disorganization. The New York Times recently reported on a landmark study that pieces together the steps by which overactive genes can increase a person’s risk of developing schizophrenia.

The researchers found that the risk of schizophrenia is tied to a natural process called synaptic pruning. As a person matures from adolescence and early adulthood, the prefrontal cortex of the brain (the section where thinking and planning skills are centered) prunes or removes weak or redundant connections between neurons. According to this study, people who are at risk for developing schizophrenia carry overactive C4-A genes that tag too many of the connections for pruning, resulting in fewer neural connections and thinner prefrontal layers, which is associated with schizophrenia.

Since the schizophrenic’s loss of frontal lobe activity is where executive functions develop, this study explains why schizophrenic adolescents have difficulty defining and adopting adult thinking. Researchers hope that completing this at-risk genetic profile will lead to clarifying a better prognosis for these people.

The more that is learned of mental disorders, the closer we are to knowing how to treat them effectively. For now, medication can blunt some of the symptoms of schizophrenia. Also psychotherapy is an effective treatment for mental disorders.

As a psychologist with over 30 years of experience in counseling families, I also see the importance of providing therapy for family members who have the ongoing stress of caring for someone with a serious mental disorder. If this describes you and you live near Portland, OR/Vancouver, WA, please contact my office and schedule an appointment to get the support and understanding that you need and deserve.