ArticleFrontiers in synaptic neuroscience2020
Excessive β-Catenin in Excitatory Neurons Results in Reduced Social and Increased Repetitive Behaviors and Altered Expression of Multiple Genes Linked to Human Autism.
Article in Frontiers in synaptic neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Unraveling the Role of Wnt Signaling Pathway in the Pathogenesis of Autism Spectrum Disorder (ASD): A Systematic Review.Molecular neurobiology · 2025Pooled it
- FMRP Regulates NrCAM Expression via β-catenin and Modulates PSD95, Dendritic Spines and Autism-like Behaviors.Neuroscience bulletin · 2026Article
- The WNT/β-catenin Pathway and Matrix Metalloproteinase-9 in hypermobile Ehlers-Danlos Syndrome and Autism Spectrum Disorder: A Possible Connection.Journal of musculoskeletal & neuronal interactions · 2026Review
- Altered expression of KCNQ1OT1 and ZEB1-AS1 lncRNAs in autism spectrum disorder: A case-control study.Molecular biology reports · 2026Article
- Review
- Serum Levels of Wnt/β-catenin Pathway Regulators Dkk-1, PORCN, Notum, and Tiki-1 in Children with Autism Spectrum Disorder.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2026Article
- CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Mechanisms of brain overgrowth in autism spectrum disorder with macrocephaly.Frontiers in neuroscience · 2025Review
- Inhibition of GSK3α,β rescues cognitive phenotypes in a preclinical mouse model of CTNNB1 syndrome.EMBO molecular medicine · 2024Article
- Assessing the COX-2/PGE2 Ratio and Anti-Nucleosome Autoantibodies as Biomarkers of Autism Spectrum Disorders: Using Combined ROC Curves to Improve Diagnostic Values.Current issues in molecular biology · 2024Article
- Cortical Parvalbumin-Positive Interneuron Development and Function Are Altered in the APC Conditional Knockout Mouse Model of Infantile and Epileptic Spasms Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- CTNNB1 in neurodevelopmental disorders.Frontiers in psychiatry · 2023Review
- Wnt/β-Catenin-Dependent Transcription in Autism Spectrum Disorders.Frontiers in molecular neuroscience · 2021Review
- Deletion of BDNF in Pax2 Lineage-Derived Interneuron Precursors in the Hindbrain Hampers the Proportion of Excitation/Inhibition, Learning, and Behavior.Frontiers in molecular neuroscience · 2021Article
- Paving the way toward treatment solutions for CTNNB1 syndrome: a patient organization perspective.Therapeutic advances in rare diseaseReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Multiple human autism risk genes are predicted to converge on the β-catenin (β-cat)/Wnt pathway. However, direct tests to link β-cat up- or down-regulation with autism are largely lacking, and the associated pathophysiological changes are poorly defined. Here we identify excessive β-cat as a risk factor that causes expression changes in several genes relevant to human autism. Our studies utilize mouse lines with β-cat dysregulation in forebrain excitatory neurons, identified as cell types with a convergent expression of autism-linked genes in both human and mouse brains. We show that mice expressing excessive β-cat display behavioral and molecular changes, including decreased social interest, increased repetitive behaviors, reduced parvalbumin and altered expression levels of additional genes identified as potential risk factors for human autism. These behavioral and molecular phenotypes are averted by reducing β-cat in neurons predisposed by gene mutations to express elevated β-cat. Using next-generation sequencing of the prefrontal cortex (PFC), we identify 87 dysregulated genes that are shared between mouse lines with excessive β-cat and autism-like behaviors, but not mouse lines with reduced β-cat and normal social behavior. Our findings provide critical new insights into β-cat, Wnt pathway dysregulation in the brain causing behavioral phenotypes relevant to the disease and the molecular etiology which includes several human autism risk genes.
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What OpenQuestion holds
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.