ArticleMolecular psychiatry2014
Adenomatous polyposis coli protein deletion leads to cognitive and autism-like disabilities.
Article in Molecular psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline 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
- Autism: epidemiology, genetics, molecular mechanisms, clinical features, diagnosis, and management.Molecular biomedicine · 2026Review
- FMRP Regulates NrCAM Expression via β-catenin and Modulates PSD95, Dendritic Spines and Autism-like Behaviors.Neuroscience bulletin · 2026Article
- APC in the nervous system.Medical molecular morphology · 2026Review
- Familial Adenomatous Polyposis-Risk of Cancer, Cancer Prevention, and Long-Term Consequences: Learnings from Five Decades with the Danish Polyposis Register.APMIS : acta pathologica, microbiologica, et immunologica Scandinavica · 2026Review
- Roles of Wnt/β-Catenin Signaling in Osteoporosis, Disease Pathogenesis, and Natural Compound Intervention.Biomolecules & therapeutics · 2026Review
- CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- Familial adenomatous polyposis family with clustering of psychiatric disorders.Japanese journal of clinical oncology · 2025Article
- Two independent families with de novo whole APC gene deletion and intellectual disability: a case report.Hereditary cancer in clinical practice · 2025Article
- Wnt/β-catenin signaling pathway: proteins' roles in osteoporosis and cancer diseases and the regulatory effects of natural compounds on osteoporosis.Molecular medicine (Cambridge, Mass.) · 2024Review
- Inhibition of GSK3α,β rescues cognitive phenotypes in a preclinical mouse model of CTNNB1 syndrome.EMBO molecular medicine · 2024Article
- Rare Germline Variants in the Adenomatous Polyposis Coli Gene Associated with Dental and Osseous Anomalies.International journal of molecular sciences · 2024Review
- Gestational Fisetin Exerts Neuroprotection by Regulating Mitochondria-Directed Canonical Wnt Signaling, BBB Integrity, and Apoptosis in Prenatal VPA-Induced Rodent Model of Autism.Molecular neurobiology · 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
- Article
- Nonmalignant Features Associated with Inherited Colorectal Cancer Syndromes-Clues for Diagnosis.Cancers · 2022Review
- Generalized and social anxiety disorder interactomes show distinctive overlaps with striosome and matrix interactomes.Scientific reports · 2021Article
- Dissecting Molecular Genetic Mechanisms of 1q21.1 CNV in Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- The role of GABAergic signalling in neurodevelopmental disorders.Nature reviews. 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
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8 authors at 1 institution in 1 country.
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Abstract
Intellectual disabilities (IDs) and autism spectrum disorders link to human APC inactivating gene mutations. However, little is known about adenomatous polyposis coli's (APC's) role in the mammalian brain. This study is the first direct test of the impact of APC loss on central synapses, cognition and behavior. Using our newly generated APC conditional knock-out (cKO) mouse, we show that deletion of this single gene in forebrain neurons leads to a multisyndromic neurodevelopmental disorder. APC cKO mice, compared with wild-type littermates, exhibit learning and memory impairments, and autistic-like behaviors (increased repetitive behaviors, reduced social interest). To begin to elucidate neuronal changes caused by APC loss, we focused on the hippocampus, a key brain region for cognitive function. APC cKO mice display increased synaptic spine density, and altered synaptic function (increased frequency of miniature excitatory synaptic currents, modestly enhanced long-term potentiation). In addition, we found excessive β-catenin levels and associated changes in canonical Wnt target gene expression and N-cadherin synaptic adhesion complexes, including reduced levels of presenilin1. Our findings identify some novel functional and molecular changes not observed previously in other genetic mutant mouse models of co-morbid cognitive and autistic-like disabilities. This work thereby has important implications for potential therapeutic targets and the impact of their modulation. We provide new insights into molecular perturbations and cell types that are relevant to human ID and autism. In addition, our data elucidate a novel role for APC in the mammalian brain as a hub that links to and regulates synaptic adhesion and signal transduction pathways critical for normal cognition and behavior.
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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.