Metformin ameliorates core deficits in a mouse model of fragile X syndrome
Nature Medicine 23, 674 (2017).
doi:10.1038/nm.4335
Authors: Ilse Gantois, Arkady Khoutorsky, Jelena Popic, Argel Aguilar-Valles, Erika Freemantle, Ruifeng Cao, Vijendra Sharma, Tine Pooters, Anmol Nagpal, Agnieszka Skalecka, Vinh T Truong, Shane Wiebe, Isabelle A Groves, Seyed Mehdi Jafarnejad, Clément Chapat, Elizabeth A McCullagh, Karine Gamache, Karim Nader, Jean-Claude Lacaille, Christos G Gkogkas & Nahum Sonenberg
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 Fmr1−/y mice and selectively normalizes ERK signaling, eIF4E phosphorylation and the expression of MMP-9. Thus, metformin is a potential FXS therapeutic.
Source: Nature Medicine - Category: General Medicine Authors: Ilse Gantois Arkady Khoutorsky Jelena Popic Argel Aguilar-Valles Erika Freemantle Ruifeng Cao Vijendra Sharma Tine Pooters Anmol Nagpal Agnieszka Skalecka Vinh T Truong Shane Wiebe Isabelle A Groves Seyed Mehdi Jafarnejad Cl é ment Chapat Elizabeth A McC Tags: Brief Communication Source Type: research
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