Our research follows the central hypothesis that de novo protein synthesis in neurons is a fundamental requirement for learning, and dysregulation of this process is a core contributor to autism and intellectual disability (ASD/ID). Our research questions are being investigated in multiple neural circuits using biochemical, electrophysiological and systems-level approaches.
Current projects include:
Molecular profiling of epileptic circuits in models of Fragile X and SYNGAP1 haploinsufficiency
Multi-omics analysis of synaptic protein turnover in mutant models of autism
Tracking activity dependent changes in mRNA translation using cell type-specific TRAP-seq
We are studying these basic biological questions using animal models of Fragile X Syndrome, SYNGAP1 Happloinsufficency, Tuberous Sclerosis, and other neurodevelopmental disorders. It is our belief that identifying the mechanisms that go awry in these models will simultaneously address fundamental questions of synaptic function, and provide a better understanding of autism and ID.
tdTom filled TRAP neurons