Lovastatin corrects excess protein synthesis and prevents epileptogenesis in a mouse model of fragile X syndrome

Neuron. 2013 Jan 23;77(2):243-50. doi: 10.1016/j.neuron.2012.01.034.

Abstract

Many neuropsychiatric symptoms of fragile X syndrome (FXS) are believed to be a consequence of altered regulation of protein synthesis at synapses. We discovered that lovastatin, a drug that is widely prescribed for the treatment of high cholesterol, can correct excess hippocampal protein synthesis in the mouse model of FXS and can prevent one of the robust functional consequences of increased protein synthesis in FXS, epileptogenesis. These data suggest that lovastatin is potentially disease modifying and could be a viable prophylactic treatment for epileptogenesis in FXS.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Disease Models, Animal*
  • Epilepsy / genetics
  • Epilepsy / metabolism
  • Epilepsy / prevention & control*
  • Fragile X Syndrome / drug therapy*
  • Fragile X Syndrome / genetics
  • Fragile X Syndrome / metabolism
  • Lovastatin / pharmacology
  • Lovastatin / therapeutic use*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Protein Biosynthesis / drug effects*
  • Protein Biosynthesis / physiology

Substances

  • Lovastatin