ArticleScientific reports2019
Altered spinogenesis in iPSC-derived cortical neurons from patients with autism carrying de novo SHANK3 mutations.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 69 citations in OpenAlex.
- Characterization of Electrophysiological and Transcriptomic Alterations in Patient-Derived Neurons from CHAMP1 Syndrome.bioRxiv : the preprint server for biology · 2026Article
- "SHANK3 deficiency alters early progenitor dynamics and reveals shared pathways with neurodegeneration".Molecular psychiatry · 2026Article
- Glycine-modulating Slc6a20a-ASO restores NMDA receptor function in SHANK2 and SHANK3-mutant mice and cortical organoids.Nature communications · 2026Article
- Male caregiving experience alters hippocampal neuroplasticity and transcription independent of reproduction in a biparental species.Communications biology · 2025Article
- Shank3 mutation impairs glutamate signaling and myelination in ASD mouse model and human iPSC-derived OPCs.Science advances · 2024Article
- Low-level brain somatic mutations in exonic regions are collectively implicated in autism with germline mutations in autism risk genes.Experimental & molecular medicine · 2024Article
- Pharmacological modulation of developmental and synaptic phenotypes in human SHANK3 deficient stem cell-derived neuronal models.Translational psychiatry · 2024Article
- Filopodial protrusion driven by density-dependent Ena-TOCA-1 interactions.Journal of cell science · 2024Article
- Impaired synaptic function and hyperexcitability of the pyramidal neurons in the prefrontal cortex of autism-associated Shank3 mutant dogs.Molecular autism · 2024Article
- Article
- Oxytocin protective effects on zebrafish larvae models of autism-like spectrum disorder.Iranian journal of basic medical sciences · 2023Article
- Functional maturation of human iPSC-derived pyramidal neuronsFrontiers in cellular neuroscience · 2023Article
- Haploinsufficiency of Shank3 increases the orientation selectivity of V1 neurons.Scientific reports · 2022Article
- Article
- Modeling human telencephalic development and autism-associated SHANK3 deficiency using organoids generated from single neural rosettes.Nature communications · 2022Article
- Unraveling pathological mechanisms in neurological disorders: the impact of cell-based and organoid models.Neural regeneration research · 2022Review
- Association of SHANK Family with Neuropsychiatric Disorders: An Update on Genetic and Animal Model Discoveries.Cellular and molecular neurobiology · 2022Review
- Signalling pathways in autism spectrum disorder: mechanisms and therapeutic implications.Signal transduction and targeted therapy · 2022Review
- iPSC toolbox for understanding and repairing disrupted brain circuits in autism.Molecular psychiatry · 2022Review
- The Synaptic Gene Study: Design and Methodology to Identify Neurocognitive Markers in Phelan-McDermid Syndrome andFrontiers in neuroscience · 2022Article
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The synaptic protein SHANK3 encodes a multidomain scaffold protein expressed at the postsynaptic density of neuronal excitatory synapses. We previously identified de novo SHANK3 mutations in patients with autism spectrum disorders (ASD) and showed that SHANK3 represents one of the major genes for ASD. Here, we analyzed the pyramidal cortical neurons derived from induced pluripotent stem cells from four patients with ASD carrying SHANK3 de novo truncating mutations. At 40-45 days after the differentiation of neural stem cells, dendritic spines from pyramidal neurons presented variable morphologies: filopodia, thin, stubby and muschroom, as measured in 3D using GFP labeling and immunofluorescence. As compared to three controls, we observed a significant decrease in SHANK3 mRNA levels (less than 50% of controls) in correlation with a significant reduction in dendritic spine densities and whole spine and spine head volumes. These results, obtained through the analysis of de novo SHANK3 mutations in the patients' genomic background, provide further support for the presence of synaptic abnormalities in a subset of patients with ASD.
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