Syracuse Sun

The neocortex, which is responsible for decision-making, sensory processing, and memory in humans, accounts for more than 75% of the brain's volume. Disruptions in its development can lead to neurodevelopmental disorders such as autism spectrum disorders, intellectual disability, and schizophrenia. The causes of these disruptions are not fully understood but are believed to involve genetic and environmental factors, including maternal nutrition during pregnancy.

Jessica MacDonald, an associate professor of biology at the College of Arts and Sciences, has been awarded a two-year grant from the National Institutes of Health to study the effects of maternal folic acid supplementation on neocortex development. MacDonald was inspired by previous findings that indicated folic acid supplementation during the first trimester significantly reduces the risk of neural tube closure defects like spina bifida.

“In countries where cereals and grains have been routinely fortified by folic acid, the incidence rate of neural tube closure defects has dropped 30% overall,” says MacDonald. She explains that whether folic acid supplementation prevents these defects depends on their initial cause and specific genetic mutations.

Previous research using mice with genetic mutations showed that higher maternal folic acid levels during gestation decreased neural tube defect rates significantly. MacDonald's team will investigate if similar benefits apply to disrupted neocortical development in mice.

“Our preliminary data are very promising that this will occur,” says MacDonald. She notes that studies suggest maternal folic acid supplementation later in pregnancy might reduce neurodevelopmental and neuropsychiatric disorders such as autism and schizophrenia. However, excessive folic acid could be harmful depending on individual genetics.

Graduate student Sara Brigida will lead this project in MacDonald's lab with assistance from both graduate and undergraduate students as they explore how maternal folic acid affects neocortical development and influences typical versus atypical neurodevelopment.