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ICAM5 as a Novel Target for Treating Cognitive Impairment in
AAV-shRNA virus (From BrainVTA) was used for suppressing ICAM5 expression to verify the involvement of ICAM5 in dendritic spines.
The viruses used in this article from BrainVTA are in the table below
Pub Date : 2019-09-19, DOI: 10.1002/advs.201901240   Email:
Ya-ping Pei,Yue-yiWang, Dan Liu, Hui-yang Lei, Zhi-hao Yang, Zi-wei Zhang, Man Han, Ke Cheng, Yu-shan Chen, Jin-quan Li, Gui-rong Cheng, Lang Xu, Qing-mingWu, ShawnM.McClintock, Ying Yang, Yong Zhang, and Yan Zeng
Fragile X syndrome (FXS) is the most common inherited form of intellectual disability, resulted from the silencing of the Fmr1 gene and the subsequent loss of fragile X mental retardation protein (FMRP). Spine dysgenesis and cognitive impairment have been extensively characterized in FXS; however, the underlying mechanism remains poorly understood. As an important regulator of spine maturation, intercellular adhesion molecule 5 (ICAM5) mRNA may be one of the targets of FMRP and involved in cognitive impairment in FXS. Here we show that in Fmr1 KO male mice, ICAM5 was excessively expressed during the late developmental stage, and its expression was negatively correlated with the expression of FMRP and positively related with the morphological abnormalities of dendritic spines. While in vitro reduction of ICAM5 normalized dendritic spine abnormalities in Fmr1 KO neurons, and in vivo knockdown of ICAM5 in the dentate gyrus rescued the impaired spatial and fear memory and anxiety-like behaviors in Fmr1 KO mice, through both granule cell and mossy cell with a relative rate of 1.320.15. Furthermore, biochemical analyses showed direct binding of FMRP with ICAM5mRNA, to the coding sequence of ICAM5 mRNA. Together, our study suggests that ICAM5 is one of the targets of FMRP and is implicated in the molecular pathogenesis of FXS. ICAM5 could be a therapeutic target for treating cognitive impairment in FXS.

Fig.1 ICAM5 knockdown improved the locomotor or anxiety-like behaviors in Fmr1 KO mice. 
To examine a possible link between ICAM5 and FMRP in FXS, and to further investigate the molecular detail and the pathological consequences, using gene overexpression, knockout and knockdown technologies (From BrainVTA) in Fmr1 KO male mice and biochemical assays, the study suggests that ICAM5 is one of the targets of FMRP and is implicated in the molecular pathogenesis of FXS. Which demonstrates the therapeutic value of ICAM5 for treating cognitive dysfunctions in FXS.

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