ReviewBrain and behavior2018
Autism throughout genetics: Perusal of the implication of ion channels.
Review in Brain and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis 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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- Metal Dyshomeostasis as a Driver of Gut Pathology in Autism Spectrum Disorders.Journal of neurochemistry · 2025Pooled it
- Characterization of Electrophysiological and Transcriptomic Alterations in Patient-Derived Neurons from CHAMP1 Syndrome.bioRxiv : the preprint server for biology · 2026Article
- Novel mouse line with D277N mutation in theFrontiers in cell and developmental biology · 2026Article
- Protein-Altering Variants' Analysis in Autism Subgroups Uncovers Early Brain-Expressed Gene Modules Relevant to Autism Pathophysiology.Autism research : official journal of the International Society for Autism Research · 2025Article
- Autism Spectrum Disorder and Epilepsy: Pathogenetic Mechanisms and Therapeutic Implications.Journal of clinical medicine · 2025Review
- Developmental deficits, synapse and dendritic abnormalities in a Clcn4 KO autism mice model: endophenotypic target for ASD.Translational psychiatry · 2025Article
- A deep learning model for prediction of autism status using whole-exome sequencing data.PLoS computational biology · 2024Article
- AST-001 Improves Social Deficits and Restores Dopamine Neuron Activity in a Mouse Model of Autism.Biomedicines · 2023Article
- Convergent coexpression of autism-associated genes suggests some novel risk genes may not be detectable in large-scale genetic studies.Cell genomics · 2023Article
- Higher scores on autonomic symptom scales in pediatric patients with neurodevelopmental disorders of known genetic etiology.Brain and behavior · 2022Article
- Shared and Cell-Type-Specific Gene Expression Patterns Associated With Autism Revealed by Integrative Regularized Non-Negative Matrix Factorization.Frontiers in genetics · 2022Article
- Ionic Channels as Potential Targets for the Treatment of Autism Spectrum Disorder: A Review.Current neuropharmacology · 2022Review
- Why not try to predict autism spectrum disorder with crucial biomarkers in cuproptosis signaling pathway?Frontiers in psychiatry · 2022Article
- Article
- A prospective birth cohort study on cord blood folate subtypes and risk of autism spectrum disorder.The American journal of clinical nutrition · 2020Article
- Article
- Disregulation of Autophagy in the Transgenerational Cc2d1a Mouse Model of Autism.Neuromolecular medicine · 2020Article
- Article
- Transcriptional Regulation of Channelopathies in Genetic and Acquired Epilepsies.Frontiers in cellular neuroscience · 2019Review
- The Relevance of Variants With Unknown Significance for Autism Spectrum Disorder Considering the Genotype-Phenotype Interrelationship.Frontiers in psychiatry · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutism spectrum disorder (ASD) comprises a group of neurodevelopmental psychiatric disorders characterized by deficits in social interactions, interpersonal communication, repetitive and stereotyped behaviors and may be associated with intellectual disabilities. The description of ASD as a synaptopathology highlights the importance of the synapse and the implication of ion channels in the etiology of these disorders.
methodsA narrative and critical review of the relevant papers from 1982 to 2017 known by the authors was conducted.
resultsGenome-wide linkages, association studies, and genetic analyses of patients with ASD have led to the identification of several candidate genes and mutations linked to ASD. Many of the candidate genes encode for proteins involved in neuronal development and regulation of synaptic function including ion channels and actors implicated in synapse formation. The involvement of ion channels in ASD is of great interest as they represent attractive therapeutic targets. In agreement with this view, recent findings have shown that drugs modulating ion channel function are effective for the treatment of certain types of patients with ASD.
conclusionThis review describes the genetic aspects of ASD with a focus on genes encoding ion channels and highlights the therapeutic implications of ion channels in the treatment of ASD.
Indexed as
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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.