Therapeutic implications of the mGluR theory of fragile X mental retardation

  • Bear M
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Evidence is reviewed that the consequences of group 1 metabotropic glutamate receptor (Gp1 mGluR) activation are exaggerated in the absence of the fragile X mental retardation protein, likely reflecting altered dendritic protein synthesis. Abnormal mGluR signaling could be responsible for remarkably diverse psychiatric and neurological symptoms in fragile X syndrome, including delayed cognitive development, seizures, anxiety, movement disorders and obesity.

Author-supplied keywords

  • Animals
  • Anxiety Disorders/genetics/metabolism/physiopathol
  • Brain/*metabolism/physiopathology
  • Child
  • Developmental Disabilities/genetics/metabolism/phy
  • Epilepsy/genetics/metabolism/physiopathology
  • Fragile X Mental Retardation Protein
  • Fragile X Syndrome/*metabolism/physiopathology/the
  • Humans
  • Movement Disorders/genetics/metabolism/physiopatho
  • Nerve Tissue Proteins/genetics/*metabolism
  • RNA-Binding Proteins/genetics/*metabolism
  • Receptors, Metabotropic Glutamate/*biosynthesis

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  • M F Bear

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