ArticleThe Journal of experimental medicine2022
FGFR3 overactivation in the brain is responsible for memory impairments in Crouzon syndrome mouse model.
Article in The Journal of experimental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Fgfr3-Wnt signaling crosstalk is involved in maintaining cranial suture integrity.Bone research · 2026Article
- Pathogenic Role of FGFR3 Autoantibodies in Small Fiber Neuropathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Impaired hippocampal neurogenesis associated with regulatory ceRNA network in a mouse model of postoperative cognitive dysfunction.BMC anesthesiology · 2025Article
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- From FGFR2 mutations to precision management: a review of prenatal diagnosis and multidisciplinary interventions in apert syndrome.Frontiers in pediatrics · 2025Review
- New CRISPR/Cas9-based Fgfr2Journal of molecular medicine (Berlin, Germany) · 2024Article
- Alzheimer's disease associated isoforms of human CD33 distinctively modulate microglial cell responses in 5XFAD mice.Molecular neurodegeneration · 2024Article
- Fibroblast growth factor receptor inhibitors mitigate the neuropathogenicity ofFrontiers in immunology · 2024Article
- Technical evolution of pediatric neurosurgery: craniosynostosis from 1972 to 2023 and beyond.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2023Review
- Candidate genes for obstructive sleep apnea in non-syndromic children with craniofacial dysmorphisms - a narrative review.Frontiers in pediatrics · 2023Review
Corrections and comments
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Authors and funding
19 authors at 9 institutions in 4 countries.
Funding
Abstract
Crouzon syndrome with acanthosis nigricans (CAN, a rare type of craniosynostosis characterized by premature suture fusion and neurological impairments) has been linked to a gain-of-function mutation (p.Ala391Glu) in fibroblast growth factor receptor 3 (FGFR3). To characterize the CAN mutation's impact on the skull and on brain functions, we developed the first mouse model (Fgfr3A385E/+) of this syndrome. Surprisingly, Fgfr3A385E/+ mice did not exhibit craniosynostosis but did show severe memory impairments, a structurally abnormal hippocampus, low activity-dependent synaptic plasticity, and overactivation of MAPK/ERK and Akt signaling pathways in the hippocampus. Systemic or brain-specific pharmacological inhibition of FGFR3 overactivation by BGJ398 injections rescued the memory impairments observed in Fgfr3A385E/+ mice. The present study is the first to have demonstrated cognitive impairments associated with brain FGFR3 overactivation, independently of skull abnormalities. Our results provide a better understanding of FGFR3's functional role and the impact of its gain-of-function mutation on brain functions. The modulation of FGFR3 signaling might be of value for treating the neurological disorders associated with craniosynostosis.
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