ReviewJournal of neurodevelopmental disorders2016
Wnt signaling networks in autism spectrum disorder and intellectual disability.
Review in Journal of neurodevelopmental disorders, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 3 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed, 3 syntheses or guidelines pooled it, 187 citations in OpenAlex.
- Connecting DCX, COMT and FMR1 in social behavior and cognitive impairment.Behavioral and brain functions : BBF · 2022Pooled it
- Toxic Effects of Glyphosate on the Nervous System: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- The involvement of the canonical Wnt-signaling receptor LRP5 and LRP6 gene variants with ADHD and sexual dimorphism: Association study and meta-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019Pooled it
- Elucidating the role of DEAF1 in neurodevelopment and shared molecular pathways in high-risk autism genes using cortical organoids.Science advances · 2026Article
- USP34 Haploinsufficiency as a Cause of Neurodevelopmental Phenotypes.Clinical genetics · 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
- Pathological disruption of CELF2 shuttling causes neuronal hyperactivity, learning deficits, and seizures.The Journal of clinical investigation · 2026Article
- Functional impact of genetic background on variable expressivity in neurodevelopmental disorders.Nature communications · 2026Article
- Unraveling the Genetic and Molecular Architecture of Autism Spectrum Disorder: Implications for Clinical Genetics and Genomic Diagnostics.International journal of molecular sciences · 2026Review
- 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
- Identification of a Novel Missense Homozygous Variant in LINS1 in Two Distinct Iranian Families With Consanguineous Marriage.Molecular genetics & genomic medicine · 2026Article
- From genes to networks: neurobiological bases of neurodiversity across common developmental disorders.Frontiers in neuroscience · 2026Review
- β-catenin deficiency in forebrain excitatory neurons induces fear memory deficits and physiological alterations.Brain communications · 2026Article
- Interrogating the Regulatory Function of HAQERs during Human Cortical Development.bioRxiv : the preprint server for biology · 2025Article
- A spatial transcriptomic atlas of autism-associated genes identifies convergence in the developing human thalamus.bioRxiv : the preprint server for biology · 2025Article
- ZMYND11 functions in bimodal regulation of latent genes and brain-like splicing to safeguard corticogenesis.Nature communications · 2025Article
- ZNRF3 in neurodevelopmental disorders: insights into Wnt signaling and therapeutic potential.Neurogenetics · 2025Review
- An integrated framework for functional dissection of variable expressivity in genetic disorders.medRxiv : the preprint server for health sciences · 2025Article
- Disrupted diencephalon development and neuropeptidergic pathways in zebrafish with autism-risk mutations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Excess Wnt in neurological disease.The Biochemical journal · 2025Review
37 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGenetic factors play a major role in the risk for neurodevelopmental disorders such as autism spectrum disorders (ASDs) and intellectual disability (ID). The underlying genetic factors have become better understood in recent years due to advancements in next generation sequencing. These studies have uncovered a vast number of genes that are impacted by different types of mutations (e.g., de novo, missense, truncation, copy number variations). ABSTRACT: Given the large volume of genetic data, analyzing each gene on its own is not a feasible approach and will take years to complete, let alone attempt to use the information to develop novel therapeutics. To make sense of independent genomic data, one approach is to determine whether multiple risk genes function in common signaling pathways that identify signaling "hubs" where risk genes converge. This approach has led to multiple pathways being implicated, such as synaptic signaling, chromatin remodeling, alternative splicing, and protein translation, among many others. In this review, we analyze recent and historical evidence indicating that multiple risk genes, including genes denoted as high-confidence and likely causal, are part of the Wingless (Wnt signaling) pathway. In the brain, Wnt signaling is an evolutionarily conserved pathway that plays an instrumental role in developing neural circuits and adult brain function.
conclusionsWe will also review evidence that pharmacological therapies and genetic mouse models further identify abnormal Wnt signaling, particularly at the synapse, as being disrupted in ASDs and contributing to disease pathology.
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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.