Abstract
The “mGluR theory” has had a significant impact on the study of fragile X syndrome (FXS), and has shifted the prevailing wisdom regarding the treatment of neurodevelopmental disorders in general. When it was introduced 15 years ago, the idea that a genetically defined developmental disorder with widespread changes in brain function could be substantially improved by targeting a single biochemical pathway was considered to be quite radical. That this treatment could be effective in treating adult patients after the onset of symptoms was deemed ludicrous. This justifiable skepticism has faded in the face of a mountain of evidence from animal models that it is indeed possible to correct many severe structural, biochemical, electrophysiological, and behavioral phenotypes by inhibiting metabotropic glutamate receptor 5 (mGlu5) and the downstream biochemical pathways that couple it to FMRP-regulated neuronal protein synthesis. This chapter will summarize the mGluR theory and discuss the implications for FXS research and treatment.
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