US Pharm. 2013;38(1):HS-18.
Research conducted at the George Washington (GW) University and published in the journal Proceedings of the National Academy of Sciences (PNAS) shows that genetic lesions linked to autism and other behavioral diseases disrupt cellular and molecular mechanisms that ensure normal development of the interneuron, a key cortical neuron.
For nearly the past decade, Anthony-Samuel LaMantia, PhD, professor of pharmacology and physiology at the GW School of Medicine and Health Sciences and director of the GW Institute for Neuroscience, and colleagues have been investigating how behavioral disorders such as autism, attention-deficit/hyperactivity disorder, and schizophrenia arise during early brain development. His work focuses on diminished 22q11.2 gene dosage and its effect on cortical circuit development.
Earlier, LaMantia and his colleagues had found that one type of cortical neuron, the projection neuron, is not generated in appropriate numbers during development in a mouse model of 22q11 deletion syndrome. In the current study, LaMantia found that interneurons are not able to move properly into the cortex due to diminished expression of activity of a key regulatory pathway for migration, the CXCR4 cytokine receptor.
