Work

Selective inhibition of glycogen synthase kinase 3α corrects pathophysiology in a mouse model of fragile X syndrome

Year: 2020

Type: article

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.

Source: Science Translational Medicine

DOI: 10.1126/scitranslmed.aam8572

Authors: 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 Madison, Jeffrey R. Cottrell, Kimberly M. Huber, Edward M. Scolnick, Edward B. Holson, Florence F. Wagner, Mark F. Bear

Institutions: Massachusetts Institute of Technology, Broad Institute, Stanley Center for Psychiatric Research, The University of Texas Southwestern Medical Center

Language: English

Topic: Genetics and Neurodevelopmental Disorders

Subfield: Genetics

Field: Biochemistry, Genetics and Molecular Biology

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: green

Funders: FRAXA Research Foundation, Simons Foundation, Simons Foundation Autism Research Initiative, National Institutes of Health, Stanley Center for Psychiatric Research, Broad Institute, National Institute of Mental Health, Eunice Kennedy Shriver National Institute of Child Health and Human Development

Awards: Synaptic pathophysiology of the 16p11.2 microdeletion mouse model, Training Program in the Neurobiology of Learning and Memory, G4886216760, G7318709022, Mechanisms of neocortical and sensory hyperexcitability in Fragile X Syndrome

OpenAlex ID: W3028560525

FWCI: 5.858

Cites: 109

Cited by: 59

Related to: 10