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.

Previous research has indirectly targeted protein synthesis by seeking to temper, but not block, this process. The NYU researchers, by contrast, sought a more fundamental intervention—removing the enzyme, p70 ribosomal S6 kinase 1, or S6K1, which has previously been shown to regulate protein synthesis in FXS mice. By addressing this phenomenon at the molecular level, they hoped to diminish many of the conditions associated with FXS.