Longitudinal PET studies of mGluR5 in FXS using an FMR1 knockout mouse model.
FXS
[18F]FPEB
metabotropic glutamate receptor 5
mouse model
positron emission tomography
Journal
Translational neuroscience
ISSN: 2081-3856
Titre abrégé: Transl Neurosci
Pays: Germany
ID NLM: 101550327
Informations de publication
Date de publication:
01 Jan 2022
01 Jan 2022
Historique:
received:
04
02
2022
revised:
28
03
2022
accepted:
04
04
2022
entrez:
18
5
2022
pubmed:
19
5
2022
medline:
19
5
2022
Statut:
epublish
Résumé
Fragile X syndrome (FXS) is a monogenic disorder characterized by intellectual disability and behavioral challenges. It is caused by aberrant methylation of the fragile X mental retardation 1 (FMR1) gene. Given the failure of clinical trials in FXS and growing evidence of a role of metabotropic glutamate subtype 5 receptors (mGluR5) in the pathophysiology of the disorder, we investigated mGluR5 function in FMR1 Knockout (FMR1-KO) mice and age- and sex-matched control mice using longitudinal positron emission tomography (PET) imaging to better understand the disorder. The studies were repeated at four time points to examine age- and disease-induced changes in mGluR5 availability using 3-fluoro-[
Identifiants
pubmed: 35582646
doi: 10.1515/tnsci-2022-0217
pii: tnsci-2022-0217
pmc: PMC9055256
doi:
Types de publication
Journal Article
Langues
eng
Pagination
80-92Informations de copyright
© 2022 Sepideh Afshar et al., published by De Gruyter.
Déclaration de conflit d'intérêts
Conflict of interest: The authors state no conflicts of interest to disclose.
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