ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Genetic removal of matrix metalloproteinase 9 rescues the symptoms of fragile X syndrome in a mouse model.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 3 registered trials, which are not on this map. Cited by 113 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Safety and Tolerability of CTH120, First-in-human Phase I Study Encompassing Three Parts: Single and Multiple Ascending Doses and Potential Food Interaction
Assessment of Neural Biomarkers in Adult Subjects With Fragile X Syndrome and Typically Developing Subjects
Evaluation of the Safety, Tolerability, and Effectiveness of CTH120 in Adult Males With Fragile X Syndrome
Who cites it
113 citing papers in PubMed, 155 citations in OpenAlex.
- Neonatal expression of human FMRP isoform corrects cortical deficits and improves behavior in a mouse model of fragile X syndrome.Molecular therapy. Nucleic acids · 2026Article
- Human dorsal forebrain organoids show differentiation-state-specific protein secretion.iScience · 2025Article
- Sex differences in the modulation of anxiety- and depression-like behaviors by matrix metalloproteinase-9 expression levels in mice.Biology of sex differences · 2025Article
- Differential effects of sound repetition rate on auditory cortex development and behavior in fragile X syndrome mouse model.Experimental neurology · 2025Article
- Article
- A Two-Hit Approach Inducing Flurothyl Seizures in Fmr1 Knockout Mice Impacts Anxiety and Repetitive Behaviors.Brain sciences · 2024Article
- Synaptic cell adhesion molecules contribute to the pathogenesis and progression of fragile X syndrome.Frontiers in cellular neuroscience · 2024Review
- Phenotypic variability to medication management: an update on fragile X syndrome.Human genomics · 2023Review
- Blood-Brain Barrier Integrity Is Perturbed in aBiomolecules · 2023Article
- Mouse models of fragile X-related disorders.Disease models & mechanisms · 2023Review
- Targeted Treatments for Fragile X Syndrome.Advances in neurobiology · 2023Article
- The effect of single-cell knockout of Fragile X Messenger Ribonucleoprotein on synaptic structural plasticity.Frontiers in synaptic neuroscience · 2023Article
- Altered GnRH neuron and ovarian innervation characterize reproductive dysfunction linked to the Fragile X messenger ribonucleoprotein (Frontiers in endocrinology · 2023Article
- Progranulin is an FMRP target that influences macroorchidism but not behaviour in a mouse model of Fragile X Syndrome.Current research in neurobiology · 2023Article
- Fragile X Syndrome as an interneuronopathy: a lesson for future studies and treatments.Frontiers in neuroscience · 2023Review
- Clinical significance of matrix metalloproteinase-9 in Fragile X Syndrome.Scientific reports · 2022Article
- Article
- Single cell transcriptomics reveals dysregulated cellular and molecular networks in a fragile X syndrome model.PLoS genetics · 2022Article
- Targeted therapy of cognitive deficits in fragile X syndrome.Molecular psychiatry · 2022Article
- AAV-delivered diacylglycerol kinase DGKk achieves long-term rescue of fragile X syndrome mouse model.EMBO molecular medicine · 2022Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Fmr1 knock-out (ko) mice display key features of fragile X syndrome (FXS), including delayed dendritic spine maturation and FXS-associated behaviors, such as poor socialization, obsessive-compulsive behavior, and hyperactivity. Here we provide conclusive evidence that matrix metalloproteinase-9 (MMP-9) is necessary to the development of FXS-associated defects in Fmr1 ko mice. Genetic disruption of Mmp-9 rescued key aspects of Fmr1 deficiency, including dendritic spine abnormalities, abnormal mGluR5-dependent LTD, as well as aberrant behaviors in open field and social novelty tests. Remarkably, MMP-9 deficiency also corrected non-neural features of Fmr1 deficiency-specifically macroorchidism-indicating that MMP-9 dysregulation contributes to FXS-associated abnormalities outside the CNS. Further, MMP-9 deficiency suppressed elevations of Akt, mammalian target of rapamycin, and eukaryotic translation initiation factor 4E phosphorylation seen in Fmr1 ko mice, which are also associated with other autistic spectrum disorders. These findings establish that MMP-9 is critical to the mechanisms responsible for neural and non-neural aspects of the FXS phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.