ArticleScientific reports2020
Drug-responsive autism phenotypes in the 16p11.2 deletion mouse model: a central role for gene-environment interactions.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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
13 citing papers in PubMed, 18 citations in OpenAlex.
- WERF Endometriosis Phenome and Biobanking Harmonisation Project for Experimental Models in Endometriosis Research (EPHect-EM-Pain): methods to assess pain behaviour in rodent models of endometriosis.Molecular human reproduction · 2025Review
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.iScience · 2024Article
- The pleiotropic spectrum of proximal 16p11.2 CNVs.American journal of human genetics · 2024Review
- Progress towards understanding risk factor mechanisms in the development of autism spectrum disorders.Biochemical Society transactions · 2024Review
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.bioRxiv : the preprint server for biology · 2024Article
- Circuit mechanism underlying fragmented sleep and memory deficits in 16p11.2 deletion mouse model of autism.Research square · 2024Article
- 16p11.2 deletion mice exhibit compromised fronto-temporal connectivity, GABAergic dysfunction, and enhanced attentional ability.Communications biology · 2023Article
- Sleep disturbances in autism spectrum disorder: Animal models, neural mechanisms, and therapeutics.Neurobiology of sleep and circadian rhythms · 2023Review
- Genetic and environmental mouse models of autism reproduce the spectrum of the disease.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- FPT, a 2-Aminotetralin, Is a Potent Serotonin 5-HTACS chemical neuroscience · 2022Article
- Social behavior in 16p11.2 and 22q11.2 copy number variations: Insights from mice and humans.Genes, brain, and behavior · 2022Review
- Mice lacking melatonin MT2 receptors exhibit attentional deficits, anxiety and enhanced social interaction.Journal of psychopharmacology (Oxford, England) · 2021Article
- The Promise of Automated Home-Cage Monitoring in Improving Translational Utility of Psychiatric Research in Rodents.Frontiers in neuroscience · 2020Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
There are no current treatments for autism, despite its high prevalence. Deletions of chromosome 16p11.2 dramatically increase risk for autism, suggesting that mice with an equivalent genetic rearrangement may offer a valuable model for the testing of novel classes of therapeutic drug. 16p11.2 deletion (16p11.2 DEL) mice and wild-type controls were assessed using an ethological approach, with 24 h monitoring of activity and social interaction of groups of mice in a home-cage environment. The ability of the excitation/inhibition modulator N-acetyl cysteine (NAC) and the 5-HT
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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.