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:

• Creating human brain slice models of neurodevelopmental disorders

• Molecular profiling of auditory processing circuits in mouse models of Fragile X Syndrome and SYNGAP1 haploinsufficiency

• Cross-species analysis of neuronal proteostasis

• Tracking activity dependent changes in mRNA translation in mouse and human

• Testing gene therapy approaches for Fragile X Syndrome

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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.

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