Reversal of disease-related pathologies in the fragile X mouse model by selective activation of GABAB receptors with arbaclofen.

@article{Henderson2012ReversalOD,
  title={Reversal of disease-related pathologies in the fragile X mouse model by selective activation of GABAB receptors with arbaclofen.},
  author={Christina S Henderson and Lasani Sulochana Wijetunge and Mika Nakamoto Kinoshita and Matthew J. Shumway and Rebecca S. Hammond and Friso R. Postma and Christopher Brynczka and Roger Rush and Alexia M Thomas and Richard E Paylor and Stephen T Warren and Peter W. Vanderklish and Peter C. Kind and Randall L. Carpenter and Mark F. Bear and Aileen M. Healy},
  journal={Science translational medicine},
  year={2012},
  volume={4 152},
  pages={152ra128}
}
Fragile X syndrome (FXS), the most common inherited cause of intellectual disability and autism, results from the transcriptional silencing of FMR1 and loss of the mRNA translational repressor protein fragile X mental retardation protein (FMRP). Patients with FXS exhibit changes in neuronal dendritic spine morphology, a pathology associated with altered synaptic function. Studies in the mouse model of fragile X have shown that loss of FMRP causes excessive synaptic protein synthesis, which… CONTINUE READING
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