Brain Damage in Infants Has Been Linked to Overactive Immune System

Brain damage has been found in baby males whose mothers had highly active immune systems during pregnancy. An immune system can become "overactive" during pregnancy when a particularly stubborn infection needs to be fought off.

The research, which was released by scientists from Johns Hopkins Medicine, analyzed the brain activity of newly birthed mice. Prior to the birthing,  some of the subject pregnant mice were injected with a light toxin that should have no effect on the unborn children but would earn a powerful immune system response. The test mice immune systems were kept at an over-active rate for extended periods of time, simulating the immune inflammation caused by many maternal infection conditions in a pregnant human mother.

When the mice were birthed, the mice born from mothers with overactive immune systems displayed significantly degraded motor function and behavioral problems such as hyperactivity, indicating some level of brain damage. Interestingly, this was particularly clear in male mice where, as they aged, brain deficiencies were made more and more apparent.

The researchers concluded that immune system inflammation may be directly linked to the stunted development of the hippocampus, the part of the brain dedicated to memory and special navigation. Essentially, this means that children born of mothers who were severely sick while pregnant are at risk of being impaired with memory trouble and learning disabilities, which may worsen as they age and their brain continues to develop.

Still, not all of the study's results were so bleak. In an accompanying press release, researchers explained that the fact disabilities were far more common in male infants indicates there may be an underlying secretly critical to developing therapies that stop an overactive immune system from influencing an infant's brain development within the womb. Of course, more study into this mystery is required.

The study was released by Johns Hopkins Medicine on February 6.