Treatment of Fmr1-KO mice with Bay 60–7550 normalizes the social and cognitive deficits of infant and adolescent Fmr1-KO mice, increased the maturity of axons and dendritic spines of Fmr1-KO neurons and normalizes the exaggerated hippocampal m-GluR5 long-term depression of Fmr1-KO CA1 [72]. This evidence concerns the gene FMR1 and Cognitive impairment.