A pair of studies published Tuesday in the journal Translational Psychiatry indicate that maternal antibodies attacking the fetal brain could be a contributing factor in the development of autism spectrum disorder (ASD). Both studies out of the UC Davis MIND Institute build on previous research which found that a group of autoantibodies, those that trigger immune responses against the body’s molecules, are common in mothers of children diagnosed with ASD.
The first study looked into what proteins these antibodies act on during pregnancy. The researchers identified 6 proteins involved in brain development that the antibodies bind to, leading to a disruption in typical development, sometimes resulting in developmental disorders, such as autism. These proteins have been identified to be vital through various stages of neural development in the fetus, including neurogenesis, or the creation of new neurons.
Out of 246 participants who had children with autism, 23 percent were identified to have antibodies which attached to these proteins. Comparatively, out of 149 mothers with typically developing children, 1 percent were identified to have these antibodies. It should also be noted that these antibodies only have a 1 percent chance of a false positive due to their high specificity for autism risk.
The results of this study could lead to a test to identify these antibodies in pregnant mothers in order to predict their child’s risk of developing ASD. While this test would only apply to about 1 in 4 cases, it would allow parents and families to prepare for their children to enroll in early intervention and education programs at a young age.
In the second study, scientists looked at how a specific autoantibody, IgG, would act on a fetus once it crossed the placenta in primate models. IgG has been found to be present in 12 percent of mothers with children diagnosed with ASD and was also identified to attack the fetal brain.
The researchers collected blood serum from mothers with children with ASD and from those without. Three groups of rhesus moneys were used, due to their neural similarity to humans: one group was injected with the IgG serum, one group with the serum from the mothers without ASD and the third was left untreated.
Once the rhesus monkeys had given birth, each of the baby monkeys were tested longitudinally with MRI scans, as well as behavioral testing. The scientists found that the IgG group had significantly faster brain growth by the age of two and had increased white matter instead of grey matter, which is an indicator of ASD in humans. Behavioral analysis found that the IgG group displayed key hallmarks of ASD, namely social isolation from other monkeys and refusal of companionship.
This combination of neurological and behavioral changes as a result of exposure to IgG, indicates that this may also be a pathway for early testing and diagnosis in pregnant mothers.
Both of these studies, from the identification of autoantibodies which bind to proteins key to neural development, to the actual observation of neurological and behavioral changes in rhesus monkeys as a result of being injected with one of the autoantibodies, are very promising not only in the realm of early identification and diagnosis, but for potential prevention and treatment as well.
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