Objective Fragile X syndrome(FXS) is the most common cause of intellectual disability in males and the most common single gene cause of autism. Dendrite and spine abnormalities have been correlated with impaired cognitive abilities in FXS, where neurons show a high density of long, thin, and immature dendritic spines. But the causes of these malformations are not yet well understood. Intercellular adhesion molecule 5(ICAM5; Telencephalin), a protein of the Ig superfamily, has been implicated in neuronal and spine development as well as the formation and maintenance of dendritic filopodia. The present study is to examine a possible link for ICAM5 in Fmr1 knockout(KO) mice, the animal model of FXS and to futher investigate the direct interaction of FMRP and ICAM5. Methods Fmr1 knock out(K