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Autism is a pervasive developmental disorder (PDD) characterized by abnormalities in social interaction, communication, and behavior (repetitive/perseverative behaviors). The cause is unknown and treatments limited, but the disorder is of prenatal origin; children are born with autism even if the symptoms do not appear clearly enough to diagnose it until eye contact, locomotion and language fail to emerge normally. Our lab is working to better understand the causes of this disorder now estimated by the CDC to occur in 1 out of every 66 births.
Two recent epidemiological studies have shown a significant (doubling to tripling) incidence of Autism Spectrum Disorder (ASD) in children born to women who took antidepressants during pregnancy. One of the studies found that the largest fraction of risk was from selective serotonin reuptake inhibitors (SSRIs), the largest group of antidepressants. Unfortunately, studies of this type in people cannot determine which antidepressant(s) may be causing ASD (if any) or if non-SSRI antidepressants are or are not similarly associated with increased ASD risk. Nor can human studies determine the molecular mechanisms of how antidepressants alter the developing brain to increase the risk of ASD. Therefore, we are testing the effects of two SSRI and one non-SSRI antidepressant given during brain development in laboratory rats (from implantation to the end of major neurogenesis) to assess how the drugs affect brain development, neurotransmitters, receptors, and ASD-like behavior. Not only do we wish to determine how antidepressants may lead to ASD-associated changes, but if different types of antidepressants carry different risks for inducing ASD-related changes in the offspring. This large and complex set of experiments is currently in progress.
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