Selective inhibition of glycogen synthase kinase 3α corrects pathophysiology in a mouse model of fragile X syndrome
Patrick K. McCamphill, Laura J. Stoppel, Rebecca K. Senter, Michael C. Lewis, Arnold J. Heynen, David C. Stoppel, Vinay Sridhar, Katie A. Collins, Xi Shi, Jen Q. Pan, Jon M. Madison, Jeffrey R. Cottrell, Kimberly M. Huber, Edward M. Scolnick, Edward B. Holson, Florence F. Wagner, Mark F. Bear
Abstract
mice; unlike mGluR5 inhibitors, there was no evidence of tachyphylaxis or enhanced psychotomimetic-induced hyperlocomotion. GSK3α selective inhibitors may have potential as a therapeutic approach for treating fragile X syndrome.
Topics & Concepts
Fragile X syndromeGSK-3Glycogen synthaseGSK3BPathophysiologyFragile xFMR1KinaseEnzymeBiologyNeuroscienceCell biologyChemistryMedicineBiochemistryEndocrinologyGeneGeneticsGenetics and Neurodevelopmental DisordersAutism Spectrum Disorder ResearchFamily and Disability Support Research