Building on their earlier determination at the Universityof Buffalo re. how to reverse certain disruptions of neuronal communication that resulted in the rescue of autism-like behaviors in an animal model, principals of ASDDR LLC discovered how to reverse certain disruptions of neuronal communication stemming from the deletion of the Shank3 gene, which results in autism-like behaviors in an animal model. The UB scientists found that the disruption of this neuronal communication results from the dysregulation of actin filaments, a kind of cellular "highway" in the brain's prefrontal cortex, the command center for high-level executive functions and a key region implicated in ASD. The Investigators further found that once the expression or activity of certain actin regulators was returned to normal -- alloweing for the normal trafficking and functioning of important neuronal receptors - social behaviors in these mice could be restored. Subsequent research is focusing on novel therapeutic strategies for autism by finding an effective treatment for patients with ASD who have genetic deletion or loss-of-function mutations of Shank3 and studying how these findings might be applied to treating ASD when other genetic mutations are implicated.
