ArticleHuman molecular genetics2016
Deletion of CTNNB1 in inhibitory circuitry contributes to autism-associated behavioral defects.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses 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
60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 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
- Connecting DCX, COMT and FMR1 in social behavior and cognitive impairment.Behavioral and brain functions : BBF · 2022Pooled it
- A NovelClinical case reports · 2026Article
- FMRP Regulates NrCAM Expression via β-catenin and Modulates PSD95, Dendritic Spines and Autism-like Behaviors.Neuroscience bulletin · 2026Article
- Novel CTNNB1 Gene Variants in Spanish CTNNB1 Syndrome Patients: Clinical and Psychological Manifestations.Journal of autism and developmental disorders · 2026Article
- Epigenetic Dysregulation of the Wnt/β-Catenin Pathway via FTO-m6A in the mPFC Contributes to Autism-Like Behaviors.Molecular neurobiology · 2026Article
- Cognitive and Adaptive Functioning of CTNNB1 Syndrome Patients: A Comparison With Autism Spectrum Disorder and Cerebral Palsy.Journal of intellectual disability research : JIDR · 2025Article
- CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Expression study of Wnt/β-catenin signaling pathway associated lncRNAs in schizophrenia.Annals of general psychiatry · 2025Article
- Discovering functional interactions among schizophrenia-risk genes by combining behavioral genetics with cell biology.Neuroscience and biobehavioral reviews · 2024Review
- Prenatal Exposure to COVID-19 mRNA Vaccine BNT162b2 Induces Autism-Like Behaviors in Male Neonatal Rats: Insights into WNT and BDNF Signaling Perturbations.Neurochemical research · 2024Article
- Article
- Severity of Autism Spectrum Disorder Symptoms Associated with de novo Variants and Pregnancy-Induced Hypertension.Journal of autism and developmental disorders · 2024Article
- Sex, hormones and cerebrovascular function: from development to disorder.Fluids and barriers of the CNS · 2024Review
- Circadian clock crosstalks with autism.Brain and behavior · 2023Article
- The ortholog of human ssDNA-binding protein SSBP3 influences neurodevelopment and autism-like behaviors in Drosophila melanogaster.PLoS biology · 2023Article
- Axin2 coupled excessive Wnt-glycolysis signaling mediates social defect in autism spectrum disorders.EMBO molecular medicine · 2023Article
- 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability.Communications biology · 2023Article
- Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023Article
- CTNNB1 in neurodevelopmental disorders.Frontiers in psychiatry · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in β-catenin (CTNNB1) have been implicated in cancer and mental disorders. Recently, loss-of-function mutations of CTNNB1 were linked to intellectual disability (ID), and rare mutations were identified in patients with autism spectrum disorder (ASD). As a key regulator of the canonical Wnt pathway, CTNNB1 plays an essential role in neurodevelopment. However, the function of CTNNB1 in specific neuronal subtypes is unclear. To understand how CTNNB1 deficiency contributes to ASD, we generated CTNNB1 conditional knockout (cKO) mice in parvalbumin interneurons. The cKO mice had increased anxiety, but had no overall change in motor function. Interestingly, CTNNB1 cKO in PV-interneurons significantly impaired object recognition and social interactions and elevated repetitive behaviors, which mimic the core symptoms of patients with ASD. Surprisingly, deleting CTNNB1 in parvalbumin-interneurons enhanced spatial memory. To determine the effect of CTNNB1 KO in overall neuronal activity, we found that c-Fos was significantly reduced in the cortex, but not in the dentate gyrus and the amygdala. Our findings revealed a cell type-specific role of CTNNB1 gene in regulation of cognitive and autistic-like behaviors. Thus, this study has important implications for development of therapies for ASDs carrying the CTNNB1 mutation or other ASDs that are associated with mutations in the Wnt pathway. In addition, our study contributes to a broader understanding of the regulation of the inhibitory circuitry.
Indexed as
Identifiers
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.