Dr. Connor’s projects have focused on elucidating the mechanisms governing synapse development, and how synaptic dysfunction is associated with neurologic disorders. Specifically, he has been investigating the role of synaptic adhesion proteins (SAPs), and uncovering the role of these proteins in synaptic formation. His first project identified how genetic reduction in a group of SAPs yielded impaired synaptic function, synapse density and long-term memory deficits. The second project focused upon proteins called MAM domain containing glycosylphosphatidylinositol anchor proteins (MDGAs).
Dr. Connor was able to demonstrate the MDGA2 protein to be a powerful suppressor of synapse formation which may contribute to autism-like phenotypes in models. Furthermore, Dr. Connor was also able to show that loss of MDGA1 function contributes to schizophrenia through an upregulation of inhibition in the brain. Finally, Dr. Connor was able to show that the genetic reduction of the protein, leucine-rich repeat transmembrane proteins (LRRTM), specifically LRRTM4, compromises synaptic function and density, leading it to be a potential therapeutic target for improving synaptic function.Dr. Connor currently has one paper submitted to Cell, based on his work on MDGA2. He has also published one first author article in the journal, Neuropsychopharmacology, and has presented his findings at a number of conferences, including the Canadian Association for Neuroscience.