<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Muscas, Melania</style></author><author><style face="normal" font="default" size="100%">Louros, Susana R.</style></author><author><style face="normal" font="default" size="100%">Osterweil, Emily K.</style></author></authors><secondary-authors></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">Lovastatin, not Simvastatin, Corrects Core Phenotypes in the Fragile X Mouse Model</style></title><secondary-title><style face="normal" font="default" size="100%">eneuro</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019-05-01 00:00:00</style></date></pub-dates></dates><elocation-id><style  face="normal" font="default" size="100%">ENEURO.0097-19.2019</style></elocation-id><doi><style  face="normal" font="default" size="100%">10.1523/ENEURO.0097-19.2019</style></doi><volume><style face="normal" font="default" size="100%">6</style></volume><issue><style face="normal" font="default" size="100%">3</style></issue><abstract><style  face="normal" font="default" size="100%">The cholesterol-lowering drug lovastatin corrects neurological phenotypes in animal models of fragile X syndrome (FX), a commonly identified genetic cause of autism and intellectual disability (ID). The therapeutic efficacy of lovastatin is being tested in clinical trials for FX; however, the structurally similar drug simvastatin has been proposed as an alternative due to an increased potency and brain penetrance. Here, we perform a side-by-side comparison of the effects of lovastatin and simvastatin treatment on two core phenotypes in Fmr1-/y mice versus WT littermates: excessive hippocampal protein synthesis and susceptibility to audiogenic seizures (AGSs). We find that simvastatin does not correct excessive hippocampal protein synthesis in the Fmr1-/y hippocampus at any dose tested. In fact, simvastatin significantly increases protein synthesis in both Fmr1-/y and WT. Moreover, injection of simvastatin does not reduce AGS in the Fmr1-/y mouse, while lovastatin significantly reduces AGS incidence and severity versus vehicle-treated animals. These results show that unlike lovastatin, simvastatin does not correct core phenotypes in the Fmr1-/y mouse model.</style></abstract></record></records></xml>