ArticleCell2012
Pathogenic SYNGAP1 mutations impair cognitive development by disrupting maturation of dendritic spine synapses.
Article in Cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers, 2 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.
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Who cites it
223 citing papers in PubMed, 2 syntheses or guidelines pooled it, 402 citations in OpenAlex.
- Gene-level analysis reveals the genetic aetiology and therapeutic targets of schizophrenia.Nature human behaviour · 2025Pooled it
- SYNGAP-1 Mutation And Catatonia: A Case Series and Systematic Review.Journal of child and adolescent psychopharmacology · 2024Pooled it
- Disruption of FOXG1 Impairs the Development of Striatal dSPNs, Thereby Contributing to ASD-Like Phenotypes.Neuroscience bulletin · 2026Article
- Mesoscale proximity labeling at chromatin leads to identification of small molecule mechanism of action.Nature communications · 2026Article
- Genetic Rescue of Disrupted Synaptic Protein Interaction Network Dynamics Following SYNGAP1 Reactivation.Molecular & cellular proteomics : MCP · 2026Article
- The Synaptic Clock: SynGAP1 as a Molecular Timer of Postsynaptic Density Consolidation.Biomolecules · 2026Review
- Phosphoproteomic profiling reveals reversal of dysregulated kinase signaling by nitric oxide inhibition in the Shank3 mouse model of autism.Scientific reports · 2026Article
- Concordant transcriptional and morphological remodeling revealed bybioRxiv : the preprint server for biology · 2026Article
- Syngap1 Synchronizes Relative Neuronal Maturation Across Cortical Areas to Organize Distributed Functional Networks.bioRxiv : the preprint server for biology · 2026Article
- Disruption of the SYNGAP1 PDZ ligand motif accelerates differentiation of human iPSC-derived GABAergic neurons.bioRxiv : the preprint server for biology · 2026Article
- Loss of Necdin causes social deficit and aberrant synaptic function through destabilization of SynGAP.Molecular psychiatry · 2026Article
- Activation of silent synapses driven by emerging technologies: mechanisms, disease associations, and prospects for clinical translation.Frontiers in synaptic neuroscience · 2026Review
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Juvenile reinstatement of TCF4 in Pitt-Hopkins syndrome model mice reveals a critical window for genetic intervention.bioRxiv : the preprint server for biology · 2025Article
- Syngap1 and the development of murine neocortical progenitor cells.Nature communications · 2025Article
- The Endo-GeneScreen platform identifies drug-like probes that regulate endogenous protein levels within physiological contexts.Nature communications · 2025Article
- Genetic rescue of disrupted synaptic protein interaction network dynamics followingbioRxiv : the preprint server for biology · 2025Article
- AAV delivery of full-length SYNGAP1 rescues epileptic and behavioral phenotypes in a mouse model of SYNGAP1-related disorders.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Article
- Analysis of retrospective natural history data collected from patients with SYNGAP1-related disorders: a preliminary examination of the Citizen database.Orphanet journal of rare diseases · 2025Article
163 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
12 authors at 4 institutions in 1 country.
Funding
Abstract
Mutations that cause intellectual disability (ID) and autism spectrum disorder (ASD) are commonly found in genes that encode for synaptic proteins. However, it remains unclear how mutations that disrupt synapse function impact intellectual ability. In the SYNGAP1 mouse model of ID/ASD, we found that dendritic spine synapses develop prematurely during the early postnatal period. Premature spine maturation dramatically enhanced excitability in the developing hippocampus, which corresponded with the emergence of behavioral abnormalities. Inducing SYNGAP1 mutations after critical developmental windows closed had minimal impact on spine synapse function, whereas repairing these pathogenic mutations in adulthood did not improve behavior and cognition. These data demonstrate that SynGAP protein acts as a critical developmental repressor of neural excitability that promotes the development of life-long cognitive abilities. We propose that the pace of dendritic spine synapse maturation in early life is a critical determinant of normal intellectual development.
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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.