Abstract
Fragile X syndrome (FXS) is a devastating developmental disability that has profound effects on cognition, behavior, and seizure susceptibility. There are currently no treatments that target the underlying cause of the disorder, and recent clinical trials have been unsuccessful. In 2007, seminal work demonstrated that amyloid-beta protein precursor (APP) is dysregulated in Fmr1KO mice through a metabotropic glutamate receptor 5 (mGluR5)-dependent pathway. These findings raise the hypotheses that: (1) APP and/or APP metabolites are potential therapeutic targets as well as biomarkers for FXS and (2) mGluR5 inhibitors may be beneficial in the treatment of Alzheimer's disease. Herein, advances in the field over the past decade that have reproduced and greatly expanded upon these original findings are reviewed, and required experimentation to validate APP metabolites as potential disease biomarkers as well as therapeutic targets for FXS are discussed.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.