Correcting the core pathophysiological deficits in the mouse model of Fragile X Syndrome through NMDA receptor modulation

Fragile-X-Syndrome (FXS) is a debilitating disorder and the most common known cause of inherited intellectual disability. It results from a modification in the gene encoding the Fragile X Mental Retardation Protein, FMRP. FMRP plays a crucial role in how our brain cells function. In the FXS mouse model, where FMRP is reduced or absent (similar to the human condition), brain cells overexpress certain proteins that are involved in the encoding of information, which is essential for learning and memory. This project will examine whether we can reduce the expression of these proteins and restore the mechanisms underlying learning and memory.