Refining translational treatment development in fragile X syndrome: Lessons learned and future directions
Fragile X research has been very productive since the underlying genetic cause of the disease was discovered, with many studies reporting novel treatments that address neuroanatomical, electrophysiological, and behavioral features in mouse models. However, translating this to humans has proved difficult. Journal of Neurodevelopmental Disorders is proud to publish this thematic series, which examines the research to date and suggests ways to overcome some of the challenges facing Fragile X research.
This series was edited by Professor Craig Erickson (Cincinnati Children's Hospital Medical Center).
Existing literature draws links between social attention and socio-behavioural profiles in neurodevelopmental disorders. Fragile X syndrome (FXS) is associated with a known socio-behavioural phenotype of socia...
Authors:Hayley Crawford, Joanna Moss, Chris Oliver and Deborah Riby
Citation:Journal of Neurodevelopmental Disorders 2017 9:9
Fragile X syndrome (FXS) has been the neurodevelopmental disorder with the most active translation of preclinical breakthroughs into clinical trials. This process has led to a critical assessment of outcome me...
Authors:Dejan B. Budimirovic, Elizabeth Berry-Kravis, Craig A. Erickson, Scott S. Hall, David Hessl, Allan L. Reiss, Margaret K. King, Leonard Abbeduto and Walter E. Kaufmann
Citation:Journal of Neurodevelopmental Disorders 2017 9:14
Arbaclofen improved multiple abnormal phenotypes in animal models of fragile X syndrome (FXS) and showed promising results in a phase 2 clinical study. The objective of the study is to determine safety and eff...
Authors:Elizabeth Berry-Kravis, Randi Hagerman, Jeannie Visootsak, Dejan Budimirovic, Walter E. Kaufmann, Maryann Cherubini, Peter Zarevics, Karen Walton-Bowen, Paul Wang, Mark F. Bear and Randall L. Carpenter
Citation:Journal of Neurodevelopmental Disorders 2017 9:3
Fragile X Syndrome (FXS) occurs as a result of a silenced fragile X mental retardation 1 gene (FMR1) and subsequent loss of fragile X mental retardation protein (FMRP) expression. Loss of FMRP alters excitatory/i...
Authors:Tori L. Schaefer, Matthew H. Davenport, Lindsay M. Grainger, Chandler K. Robinson, Anthony T. Earnheart, Melinda S. Stegman, Anna L. Lang, Amy A. Ashworth, Gemma Molinaro, Kimberly M. Huber and Craig A. Erickson
Citation:Journal of Neurodevelopmental Disorders 2017 9:6
Our understanding of fragile X syndrome (FXS) pathophysiology continues to improve and numerous potential drug targets have been identified. Yet, current prescribing practices are only symptom-based in order t...
Authors:Craig A. Erickson, Matthew H. Davenport, Tori L. Schaefer, Logan K. Wink, Ernest V. Pedapati, John A. Sweeney, Sarah E. Fitzpatrick, W. Ted Brown, Dejan Budimirovic, Randi J. Hagerman, David Hessl, Walter E. Kaufmann and Elizabeth Berry-Kravis
Citation:Journal of Neurodevelopmental Disorders 2017 9:7
Cortical hyperexcitability due to abnormal fast-spiking inhibitory interneuron function has been documented in fmr1KO mice, a mouse model of the fragile X syndrome which is the most common single gene cause of a...
Authors:Jun Wang, Lauren E. Ethridge, Matthew W. Mosconi, Stormi P. White, Devin K. Binder, Ernest V. Pedapati, Craig A. Erickson, Matthew J. Byerly and John A. Sweeney
Citation:Journal of Neurodevelopmental Disorders 2017 9:11
Individuals with Williams syndrome (WS) exhibit an atypical social phenotype termed hypersociability. One theory accounting for hypersociability presumes an atypical function of the amygdala, which processes f...
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