ReviewOpen biology2019
Understanding intellectual disability and autism spectrum disorders from common mouse models: synapses to behaviour.
Review in Open biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
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Who cites it
41 citing papers in PubMed, 64 citations in OpenAlex.
- E/I imbalance and internal noise cause weak neural representations and face recognition challenges in ASD.Communications biology · 2026Article
- Autism-associated ARHGEF9 variants impair GABAergic synapses and ultrasonic communication by reducing gephyrin phosphorylation.Molecular psychiatry · 2026Article
- Memory processing in neurodevelopmental disorders: linking behavioral, circuits, and molecular scales.Frontiers in cellular neuroscience · 2026Review
- Cereblon-related mild intellectual disability disrupts response inhibition and uniformity of group-individual strategies.Frontiers in neuroscience · 2026Article
- Endosomal 2Cl-/H+ exchangers regulate neuronal excitability by tuning Kv7/KCNQ channel density.Brain : a journal of neurology · 2025Article
- Altered behaviour and immune response in mice with NHLRC2 p.Asp148Tyr variant.Brain, behavior, & immunity - health · 2025Article
- From Genetics to Function: the Role of ABCA12 in Autism Neurobiology.Journal of molecular neuroscience : MN · 2025Review
- Epigenetic modulation rescues neurodevelopmental deficits in Syngap1Aging cell · 2025Article
- Clinical and genetic findings in autism spectrum disorders analyzed using exome sequencing.Frontiers in psychiatry · 2025Article
- High neural noise in autism: A hypothesis currently at the nexus of explanatory power.Heliyon · 2024Review
- A zebrafish-based in vivo model of Zika virus infection unveils alterations of the glutamatergic neuronal development and NS4A as a key viral determinant of neuropathogenesis.PLoS pathogens · 2024Article
- Overexpression of Motopsin, an Extracellular Serine Protease Related to Intellectual Disability, Promotes Adult Neurogenesis and Neuronal Responsiveness in the Dentate Gyrus.Molecular neurobiology · 2024Article
- Article
- A splice acceptor variant in RGS6 associated with intellectual disability, microcephaly, and cataracts disproportionately promotes expression of a subset of RGS6 isoforms.Journal of human genetics · 2024Article
- Compromised transcription-mRNA export factor THOC2 causes R-loop accumulation, DNA damage and adverse neurodevelopment.Nature communications · 2024Article
- Neural deficits in a mouse model of PACS1 syndrome are corrected with PACS1- or HDAC6-targeting therapy.Nature communications · 2023Article
- 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability.Communications biology · 2023Article
- Comparing synaptic proteomes across five mouse models for autism reveals converging molecular similarities including deficits in oxidative phosphorylation and Rho GTPase signaling.Frontiers in aging neuroscience · 2023Article
- TRRAP-mediated acetylation on Sp1 regulates adult neurogenesis.Computational and structural biotechnology journal · 2023Article
- A perspective on molecular signalling dysfunction, its clinical relevance and therapeutics in autism spectrum disorder.Experimental brain research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Normal brain development is highly dependent on the timely coordinated actions of genetic and environmental processes, and an aberration can lead to neurodevelopmental disorders (NDDs). Intellectual disability (ID) and autism spectrum disorders (ASDs) are a group of co-occurring NDDs that affect between 3% and 5% of the world population, thus presenting a great challenge to society. This problem calls for the need to understand the pathobiology of these disorders and to design new therapeutic strategies. One approach towards this has been the development of multiple analogous mouse models. This review discusses studies conducted in the mouse models of five major monogenic causes of ID and ASDs: Fmr1, Syngap1, Mecp2, Shank2/3 and Neuroligins/Neurnexins. These studies reveal that, despite having a diverse molecular origin, the effects of these mutations converge onto similar or related aetiological pathways, consequently giving rise to the typical phenotype of cognitive, social and emotional deficits that are characteristic of ID and ASDs. This convergence, therefore, highlights common pathological nodes that can be targeted for therapy. Other than conventional therapeutic strategies such as non-pharmacological corrective methods and symptomatic alleviation, multiple studies in mouse models have successfully proved the possibility of pharmacological and genetic therapy enabling functional recovery.
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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.