Illness or infections during early pregnancy are associated with increased incidence of autism. In pregnant mice, exposure to viral or bacterial agents alters fetal brain development, and pups show behavioral changes that are analogous to features seen in autism.

Theo Palmer and his colleagues at Stanford University in California showed that the placenta is vulnerable to some types of bacterial infections. They also showed that alterations in GABRB3, a gene implicated in autism, can worsen illness-induced placental damage. It is known that two additional genetic autism risk factors, c-MET and MeCP2, are involved in placental development.

Palmer and his group aim to determine whether pregnancies become more vulnerable to maternal illness if the fetus carries an inactivating mutation in either c-MET or MeCP2. Subtle changes in placental development caused by defects in c-MET or MeCP2 may cause the placenta to be more sensitive to the immune molecules released during a maternal infection.

Palmer and his colleagues aim to determine whether a reduction in c-MET or MeCP2 results in more extensive placental damage and whether this damage correlates with more pronounced changes in fetal brain development. Although it is well known that genetics can influence vulnerability to an environmental risk factor, the potential for such synergies to underlie the development of autism have not been explored.