ReviewFrontiers in cellular neuroscience2016
SYNGAP1: Mind the Gap.
Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.
- Genetic landscape of patients with atypical absence status epilepticus: A systematic review.Epilepsia open · 2026Pooled it
- SYNGAP-1 Mutation And Catatonia: A Case Series and Systematic Review.Journal of child and adolescent psychopharmacology · 2024Pooled it
- Investigating the effects of missense mutations on the dual Ras/Rap activation mechanism of SYNGAP1 using molecular modelling.Journal of structural biology: X · 2026Article
- Biphasic sleep is a feature of sleep disturbance in SYNGAP1-RD.Sleep medicine · 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
- Missense mutations on SynGAP C2 domain impair membrane diffusion.Protein science : a publication of the Protein Society · 2026Article
- Role and Impact of theInternational journal of molecular sciences · 2026Article
- Genetic medicines for epilepsy: unlocking new avenues for seizure control.Frontiers in bioengineering and biotechnology · 2026Review
- Syngap1 and the development of murine neocortical progenitor cells.Nature communications · 2025Article
- Beyond synapses: cytoplasmic connections in brain function and evolution.Biological reviews of the Cambridge Philosophical Society · 2025Review
- Setting Up Our Lab-in-a-Box: Paving the Road Towards Remote Data Collection for Scalable Personalized Biometrics.Journal of personalized medicine · 2025Article
- Article
- Human neural organoid microphysiological systems show the building blocks necessary for basic learning and memory.Communications biology · 2025Article
- Article
- Clinical signatures of SYNGAP1-related disorders through data integration.Genetics in medicine : official journal of the American College of Medical Genetics · 2025Article
- Dissecting the genetic complexity of myalgic encephalomyelitis/chronic fatigue syndrome via deep learning-powered genome analysis.medRxiv : the preprint server for health sciences · 2025Article
- Dissociation of SYNGAP1 enzymatic and structural roles: Intrinsic excitability and seizure susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Dissociation of SYNGAP1 Enzymatic and Structural Roles: Intrinsic Excitability and Seizure Susceptibility.bioRxiv : the preprint server for biology · 2025Article
- SYNGAP1 Syndrome and the Brain Gene Registry.Genes · 2025Review
9 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
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A cardinal feature of early stages of human brain development centers on the sensory, cognitive, and emotional experiences that shape neuronal-circuit formation and refinement. Consequently, alterations in these processes account for many psychiatric and neurodevelopmental disorders. Neurodevelopment disorders affect 3-4% of the world population. The impact of these disorders presents a major challenge to clinicians, geneticists, and neuroscientists. Mutations that cause neurodevelopmental disorders are commonly found in genes encoding proteins that regulate synaptic function. Investigation of the underlying mechanisms using gain or loss of function approaches has revealed alterations in dendritic spine structure, function, and plasticity, consequently modulating the neuronal circuit formation and thereby raising the possibility of neurodevelopmental disorders resulting from synaptopathies. One such gene, SYNGAP1 (Synaptic Ras-GTPase-activating protein) has been shown to cause Intellectual Disability (ID) with comorbid Autism Spectrum Disorder (ASD) and epilepsy in children. SYNGAP1 is a negative regulator of Ras, Rap and of AMPA receptor trafficking to the postsynaptic membrane, thereby regulating not only synaptic plasticity, but also neuronal homeostasis. Recent studies on the neurophysiology of SYNGAP1, using Syngap1 mouse models, have provided deeper insights into how downstream signaling proteins and synaptic plasticity are regulated by SYNGAP1. This knowledge has led to a better understanding of the function of SYNGAP1 and suggests a potential target during critical period of development when the brain is more susceptible to therapeutic intervention.
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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.