ArticleJournal of neurodevelopmental disorders2010
The genetic basis of non-syndromic intellectual disability: a review.
Article in Journal of neurodevelopmental disorders, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 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.
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.
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Who cites it
124 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- A systematic review of the biological, social, and environmental determinants of intellectual disability in children and adolescents.Frontiers in psychiatry · 2022Pooled it
- Prenatal, Perinatal and Neonatal Risk Factors for Intellectual Disability: A Systemic Review and Meta-Analysis.PloS one · 2016Pooled it
- A cross-vertebrate brain protein interaction map identifies conserved neural and non-neural complexes.Cell reports · 2026Article
- A transient sex-biased transcriptional program shapes early postnatal L2/3 neuron development.Biology of sex differences · 2026Article
- Genetic analysis and reporting from whole-exome sequencing data in 1052 patients with intellectual disability.Journal of molecular medicine (Berlin, Germany) · 2026Article
- HomozygousThe Yale journal of biology and medicine · 2026Article
- The influence of genetic factors on education health and care plan obtainment for pupils with intellectual developmental disabilities.Scientific reports · 2026Article
- Identification of a Novel Missense Homozygous Variant in LINS1 in Two Distinct Iranian Families With Consanguineous Marriage.Molecular genetics & genomic medicine · 2026Article
- Diagnostic Yield of Genome Sequencing in an Iranian Exome-Negative Autosomal-Recessive Intellectual Disability Cohort.Human mutation · 2026Article
- Cereblon-related mild intellectual disability disrupts response inhibition and uniformity of group-individual strategies.Frontiers in neuroscience · 2026Article
- VerteBrain reveals novel neural and non-neural protein assemblies conserved across vertebrate evolution.bioRxiv : the preprint server for biology · 2025Article
- Exploring Proteomic Alterations in Intellectual Disability: Insights from Hyperlipidemia and Hyperphosphatasia Subgroups.Neuromolecular medicine · 2025Article
- Visual and auditory attention in individuals with DYRK1A and SCN2A disruptive variants.Autism research : official journal of the International Society for Autism Research · 2025Article
- Novel heterozygousFrontiers in neurology · 2025Article
- Review
- Characterizing Sensory Phenotypes of Subgroups with a Known Genetic Etiology Pertaining to Diagnoses of Autism Spectrum Disorder and Intellectual Disability.Journal of autism and developmental disorders · 2024Article
- Shared and divergent mental health characteristics of ADNP-, CHD8- and DYRK1A-related neurodevelopmental conditions.Journal of neurodevelopmental disorders · 2024Article
- A novel SMARCC1 BAFopathy implicates neural progenitor epigenetic dysregulation in human hydrocephalus.Brain : a journal of neurology · 2024Article
- Variants in ZFX are associated with an X-linked neurodevelopmental disorder with recurrent facial gestalt.American journal of human genetics · 2024Article
- Rare genomic copy number variants implicate new candidate genes for bicuspid aortic valve.PloS one · 2024Article
64 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intellectual disability (ID), also referred to as mental retardation (MR), is frequently the result of genetic mutation. Where ID is present together with additional clinical symptoms or physical anomalies, there is often sufficient information available for the diagnosing physician to identify a known syndrome, which may then educe the identification of the causative defect. However, where co-morbid features are absent, narrowing down a specific gene can only be done by 'brute force' using the latest molecular genetic techniques. Here we attempt to provide a systematic review of genetic causes of cases of ID where no other symptoms or co-morbid features are present, or non-syndromic ID. We attempt to summarize commonalities between the genes and the molecular pathways of their encoded proteins. Since ID is a common feature of autism, and conversely autistic features are frequently present in individuals with ID, we also look at possible overlaps in genetic etiology with non-syndromic ID.
Identifiers
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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.