Peer-reviewed veterinary case report
Metformin ameliorates core deficits in a mouse model of fragile X syndrome.
- Journal:
- Nature medicine
- Year:
- 2017
- Authors:
- Gantois, Ilse et al.
- Affiliation:
- Department of Biochemistry · Canada
Abstract
Fragile X syndrome (FXS) is the leading monogenic cause of autism spectrum disorders (ASD). Trinucleotide repeat expansions in FMR1 abolish FMRP expression, leading to hyperactivation of ERK and mTOR signaling upstream of mRNA translation. Here we show that metformin, the most widely used drug for type 2 diabetes, rescues core phenotypes in Fmr1mice and selectively normalizes ERK signaling, eIF4E phosphorylation and the expression of MMP-9. Thus, metformin is a potential FXS therapeutic.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/28504725/