Lovastatin Corrects Excess Protein Synthesis and Prevents Epileptogenesis in a Mouse Model of Fragile X Syndrome

被引:178
作者
Osterweil, Emily K. [1 ]
Chuang, Shih-Chieh [2 ,3 ]
Chubykin, Alexander A. [1 ]
Sidorov, Michael [1 ]
Bianchi, Riccardo [2 ,3 ]
Wong, Robert K. S. [2 ,3 ]
Bear, Mark F. [1 ]
机构
[1] MIT, Howard Hughes Med Inst, Picower Inst Learning & Memory, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA
[2] Suny Downstate Med Ctr, Robert F Furchgott Ctr Neural & Behav Sci, Brooklyn, NY 11203 USA
[3] Suny Downstate Med Ctr, Dept Physiol & Pharmacol, Brooklyn, NY 11203 USA
关键词
EPILEPTIFORM DISCHARGES; MENTAL-RETARDATION; EPILEPSY; SUPPRESSION; INDUCTION; MGLUR5; MICE; SEIZURES; STATIN;
D O I
10.1016/j.neuron.2012.01.034
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:243 / 250
页数:8
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