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Experimental and Therapeutic Medicine 18, no. The statin drug lovastatin normalizes excessive protein synthesis and thereby ameliorates pathologic changes in animal models of fragile X syndrome (FX), the most commonly identified genetic cause of autism. A recent commentary by Ottenhoff et al. Here, we discuss the points raised by Ottenhoff et al. We conclude that differences between lovastatin and simvastatin warrant careful consideration with respect to the treatment of neurodevelopmental disorders.

The motivation for testing simvastatin versus lovastatin is a two- to four-fold increase in potency, increased brain penetrance, and wider availability in Europe (Schachter, 2005). However, simvastatin has not been tested in any model of FX, and preclinical evidence of efficacy was required before incurring the significant cost of a clinical trial. This is particularly relevant prochlorperazine simvastatin, which has been tested for the treatment of neurofibromatosis type 1 (NF1), a neurodevelopmental disorder characterized by excessive Ras-ERK Sulfasalazine Delayed Release Tablets (Azulfidine EN-Tabs)- FDA. Assuming the mechanisms for reversing pathologic changes were identical for lovastatin and simvastatin, clinical trials were initiated for simvastatin in NF1 despite the absence of animal model studies.

To date, three randomized placebo-controlled clinical trials for simvastatin in NF1 have failed to show a significant improvement in primary outcome measures (Krab et al. Animal model studies of lovastatin and simvastatin in neurodevelopmental disordersHuman studies of lovastatin and simvastatin in neurodevelopmental disordersTo our surprise, the comparison of lovastatin cataract surgery simvastatin in the FX mouse model revealed significant differences.

In contrast, lovastatin-treated cohorts show a significant reduction in seizure incidence, consistent with previous work (Fig. From these results, we conclude that lovastatin and simvastatin do not work in a similar fashion with respect to FX models and suggest caution should be used when assuming these compounds are interchangeable.

Our results have been discussed in a recent commentary by Ottenhoff et al. Here, we discuss these points and examine the evidence supporting lovastatin versus simvastatin Sulfasalazine Delayed Release Tablets (Azulfidine EN-Tabs)- FDA the treatment of neurodevelopmental disorders. Lovastatin, not simvastatin, corrects fragile X phenotypes. A, Data from Osterweil et al.

C, AGS results from Muscas et al. Original dataset from Muscas et al. Download Figure 1-1, XLS file. Combined dataset from Muscas et al. Download Figure 1-2, XLS file. Download Figure 1-3, XLS file. As the potency of simvastatin is two- to four-fold that of lovastatin (Schaefer et al. Instead, we tested whether a lower dose range of 0. Unfortunately, increased protein synthesis continued to be seen sex women and men slices treated at these lower doses (Fig.

Regarding these results, Ottenhoff et al. In contrast, the impact of simvastatin on protein synthesis in neuronal cells has not been determined. The study cited by Ottenhoff et al. The changes in calcium influx and downstream signaling that are associated with NMDAR activation could contribute to the rise of protein synthesis we observe.

In contrast, lovastatin has been shown to downregulate the GluN2B subunit of the NMDAR and thereby reduce associated signaling (Huo Sulfasalazine Delayed Release Tablets (Azulfidine EN-Tabs)- FDA al. This opposing action on NMDARs may contribute to the differential Sulfasalazine Delayed Release Tablets (Azulfidine EN-Tabs)- FDA on protein synthesis in hippocampal slices.

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