Autism May Be Caused By Maternal Antibodies that Target the Fetus

Today's Autism epidemic shows that as many as one in 88 children will be diagnosed with having an Autism Spectrum Disorder (ASD), according to Psychology Today. Furthermore, it has been established that autism and ASD are caused by alterations that occur during brain development.

A new study at the University of California, Davis' MIND Institute has identified a maternal autoantibody that acts on the fetus and can begin medical problems that can ultimately cause the disorder.

Autism spectrum disorder is a range of complex neurodevelopment disorders that are usually characterized by social impairments, communication difficulties and restricted, repetitive and stereotyped patterns of behavior. Autistic disorder, sometimes called autism or classical ASD, is the most severe form of ASD, while other conditions along the spectrum include a milder form known as Asperger syndrome, and childhood disintegrative disorder and pervasive developmental disorder not otherwise specified. Males are also four times more likely to have an ASD than females, according to the Centers for Disease Control and Prevention.

During pregnancy, immune disorders can be particularly dangerous as the placenta is the only barrier between the fetus and its mother's antibodies. A mother's antibodies will cross the placenta and protect the fetus from infections. However, if autoantibodies cross the placenta, they do not protect the fetus. Instead, they attack it. In fact, the autoantibody known as IgG is found to cause ASD and is present in 12 percent of women. When this autoantibody enters the placenta, it attacks the fetus' brain.

During the study, researchers looked at rhesus monkeys to examine brain organization and cognitive and social functions as humans. Three groups were used--each composed of eight monkeys: one group was given the IgG serum from mothers of children with ASD, another was given the serum from mothers with children without ASD, and a third group was left untreated.

After birth, the baby monkeys were given longitudinal magnetic resonance imaging scans (MRI) at six months of age to check for physical developmental differences in their brains at one week, one month, three months, six months, one year and two years of age. Their behavior and social development was also observed, as a majority of ASD is characterized by an inability to develop normal social interactions.

Researchers noted that the monkeys who had received the ASD-related IgG compared to the monkeys who did not and the control group were vastly different. Brain growth was significantly faster in the IgG-ASD monkeys, who also had larger brains with more white matter than normal, which is indicative of autism. These same monkeys also exhibited behavior similar to those with autism or signs that they would soon develop autism, including antisocial behavior.

"The combination of brain and behavioral changes observed in the nonhuman primate offspring exposed to these autism-specific antibodies suggests that this is a very promising avenue of research," said Melissa D. Bauman, Ph.D., lead author of the study, "highlighting the collaborative efforts that characterize research at the UC Davis MIND Institute."

More information regarding the study can be found in Translational Psychiatry.