Researchers at the University of California found excessive neuron development in the prefrontal cortex in boys with autism. The neurons affect the part of the brain responsible for social development. Social developmental problems are one of the main characteristics of autism. According to the study, researchers found a 67% increase cortical cells in male patients with autism. Cortical cells are developed in-utero. This finding leads researchers to believe that developmental problems in-utero is the cause of autism.

The study, which was published in the Journal of the American Medical Society, supports findings from other studies resulting in the same theories on autism development. Children born with autism tend to have smaller head circumferences at birth with a sharp increase in the first year. Researchers studies brain cells in seven patients recently deceased. The boys ranged in age from two to 16 and all were diagnosed with autism before death. The cell counts of the autistic patients were compared with cell counts of six healthy boys.

Eric Courchesne, PhD has a theory about the cause of excessive cell development in the prefrontal cortex. “Brain imaging studies of young children with autism have shown overgrowth and dysfunction in the prefrontal cortex as well as other brain regions. But the underlying cause at the level of brain cells has remained a mystery. The best guess was that overgrowth of prefrontal cortex might be due to an abnormal excess of brain cells, but this had never been tested.”

In addition to excessive cells in the brain, the overall weight of the brain in the autism patients was higher than patients without autism. The increased weight could be attributed to overgrowth.

When the brain develops normally, there is excess cell development between 10 and 20 weeks gestation. Typically, the excess cells die off during the third trimester, but this may not be the case with autism. It appears that the extra cells continue to thrive and apoptosis, or cell death, does not occur.

Source: Eric Courchesne, PhD; Peter R. Mouton, PhD; Michael E. Calhoun, PhD; Katerina Semendeferi, PhD; Cielia Ahrens-Barbeau; Melodies J. Hallet; Cynthia Carter Barnes, PhD; Karen Pierce, PhD. University of California-San Diego. 10 November, 2011.