Neuroscientists at New York University have devised a method that has reduced several afflictions associated with Fragile X syndrome (FXS) in laboratory mice. Their findings, which are reported in the journal Neuron, offer new possibilities for addressing FXS, the leading inherited cause of autism and intellectual disability.
Those afflicted with FXS do not possess the protein FMRP, which is a suppressor of protein synthesis. Absent this suppressor, protein synthesis is exaggerated, producing a range of mental and physical disorders.