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.