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Publication : Inhibition of GSK3β improves hippocampus-dependent learning and rescues neurogenesis in a mouse model of fragile X syndrome.

First Author  Guo W Year  2012
Journal  Hum Mol Genet Volume  21
Issue  3 Pages  681-91
PubMed ID  22048960 Mgi Jnum  J:179694
Mgi Id  MGI:5302903 Doi  10.1093/hmg/ddr501
Citation  Guo W, et al. (2012) Inhibition of GSK3beta improves hippocampus-dependent learning and rescues neurogenesis in a mouse model of fragile X syndrome. Hum Mol Genet 21(3):681-91
abstractText  Fragile X syndrome (FXS), a common inherited form of intellectual disability with learning deficits, results from a loss of fragile X mental retardation protein (FMRP). Despite extensive research, treatment options for FXS remain limited. Since FMRP is known to play an important role in adult hippocampal neurogenesis and hippocampus-dependent learning and FMRP regulates the adult neural stem cell fate through the translational regulation of glycogen synthase kinase 3beta (GSK3beta), we investigated the effects of a GSK3beta inhibitor, SB216763, on Fmr1 knockout mice (Fmr1 KO). We found that the inhibition of GSK3beta could reverse the hippocampus-dependent learning deficits and rescue adult hippocampal neurogenesis at multiple stages in Fmr1 KO mice. Our results point to GSK3beta inhibition as a potential treatment for the learning deficits seen in FXS.
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