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Dr. Lauren Ellman, Temple University – Prenatal Flu and Schizophrenia

In today’s Academic Minute, Dr. Lauren Ellman of Temple University examines the connection between a prenatal bout with the flu and an increased rate of schizophrenia.

Lauren Ellman is an assistant professor of psychology at Temple University, where her primary research is focused on pre- and perinatal influences in neurodevelopment and the risk for major mental disorders, such as schizophrenia.  Ellman also has ongoing studies investigating risk factors for schizophrenia among older adolescents and young adults using clinical, psychosocial, and neuroimaging techniques. She holds a Ph.D. from the University of California Los Angeles.

About Dr. Ellman

Dr. Lauren Ellman – Prenatal Flu and Schizophrenia

It is now clear that maternal psychological and biological information is communicated to the fetus during pregnancy in a variety of ways and can greatly influence subsequent development. My research focuses on how a number of maternal conditions during pregnancy, including infection, malnutrition, exposure to serious life stressors (such as the loss of a close relative), are associated with risk of schizophrenia among offspring. Schizophrenia is a serious mental disorder.

Some of our most intriguing results have shown that maternal infections, such as influenza,  during pregnancy and immune responses to infection are associated with an increased risk for schizophrenia and a more severe course of the disorder. These results were derived from longitudinal cohort studies that prospectively collected obstetric information (including maternal sera during pregnancy) in the 1950’s and 60’s and then identified those who developed schizophrenia or other psychotic disorders in adulthood.

One study in particular found that maternal influenza infection during pregnancy increased the risk of schizophrenia in offspring and lead to decreases in childhood verbal IQ performance at age 7 among those who later developed schizophrenia, therefore leading to a cognitive change far before schizophrenia symptom onset.   In those children who did not go on to develop schizophrenia, no observable changes were found in IQ, suggesting that liability for schizophrenia was necessary for influenza to negatively impact the fetus.

Because most viruses do not seem to cross the placenta, the damaging effects to the fetus likely involve maternal immune responses to infection, such as increases in proteins called proinflammatory cytokines--considered the “hormones” of the immune system--that are associated with inflammation. One of our studies found that fetal exposure to increases in a proinflammatory cytokine led to significant structural brain alterations in schizophrenia cases, but not in controls.  Such neuroanatomical abnormalities are consistent with the interpretation that vulnerability for schizophrenia renders the fetal brain susceptible to infection and immune responses to infection.
 

 

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