Clemson University scientist David Feliciano recently received a three-year, $442,000 grant from the National Institutes of Health to study how alterations to a complex pathway in the developing brain cause a constellation of neurological disorders, including the simultaneous presence of autism and epilepsy. The project will test the hypothesis that a transporter of amino acids in the brain regulates the “mammalian target of rapamycin” (mTOR) pathway in newborn neurons during fetal and early postnatal development of the cerebral cortex, the outer layer of the brain responsible for integrating sensory information with thought processing.
“The research funded by this grant will be devoted to forming a greater understanding of the upstream signals that turn the mTOR pathway on and off during development,” said Feliciano, an assistant professor in the College of Science. “We already know that too much or too little mTOR pathway activity can cause neurological diseases. But no one has yet to show whether amino acids play a critical role in brain development during the perinatal period.”
A vast array of changes must successfully occur to create a healthy, fully functioning brain. But deviations in mTOR pathway activity can inhibit these developments, and to further complicate matters, clinicians currently don’t possess reliable methods of measuring this activity.
Alterations in the mTOR pathway — whether due to mutations in genes or environmental factors — are linked to neurodevelopmental malformations that might contribute to autism, epilepsy and intellectual delay.