Prenatal and early-life infections and associated febrile and immune responses may contribute to autism by regulating brain maturation and central nervous system function. W. Ian Lipkin, Mady Hornig and their colleagues at Columbia University aim to examine the role of infection and immunity in the pathogenesis of neurodevelopmental disorders. They plan to study a large pregnancy and birth cohort comprising more than 114,000 children and their parents.
The Autism Birth Cohort has detailed serially collected questionnaire data regarding exposures to illness, fever, medications and psychosocial stressors, as well as maternal reports of diet and intake of micronutrients captured in four-week intervals across all phases of pregnancy. Lipkin, Hornig and their teams plan to analyze these questionnaires to determine the significance of individual exposures and their timing during the course of neural development, as well as whether dietary or supplemental micronutrients, antipyretics or nonsteroidal anti-inflammatory agents influence risk of disease.
Immune response genes, immune state during pregnancy and prior infections may contribute to the diversity in outcomes after prenatal or early-life exposure to infection. The researchers aim to use proteomic tools to test maternal and cord blood for the presence of immune molecules that may contribute to the pathogenesis of neurodevelopmental damage or serve as biomarkers for risk. The researchers plan to survey infectious triggers for the induction of immune activation by serological testing for gestational exposure to influenza and other agents potentially implicated in autism.