Grant: CIHR Fellowship

Autistic spectrum disorders are characterized by important social deficits. Patients with autism have great difficulties establishing meaningful contact with other individuals and understanding their emotions and intentions. In addition to limiting the quality of their social interactions, these deficits impede the development of other skills that depend on inter-individual knowledge transfer. To this day, there exists no efficient treatment for social cognition problems, mainly because the neurobiology of social cognition is unknown. In this research project, I will be part of a multidisciplinary team attempting to, for one, elucidate the neurobiological mechanisms underlying social cognition, and for two, validate two promising therapeutical options to enhance social cognition. To achieve these objectives, we will require an animal model that allows studying the neurobiological mechanisms of social cognition at a cellular level: the rhesus macaque. The rhesus macaque has a vast and elaborate social behavioral repertoire similar to that of humans, as opposed to rodents who are vastly used in other neuroscience applications. Moreover, the macaque brain is largely similar to the human brain, both at an anatomical and functional level. This last point is crucial because it allows to easily translate the knowledge acquired with this animal model to potential applications in humans. Ultimately, this research project will allow better understanding the neurobiological basis of social cognition and will validate promising therapeutical avenues for social deficits in humans with autistic spectrum disorders.