ReviewMammalian genome : official journal of the International Mammalian Genome Society2007
The power of comparative and developmental studies for mouse models of Down syndrome.
Review in Mammalian genome : official journal of the International Mammalian Genome Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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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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
26 citing papers in PubMed, 48 citations in OpenAlex.
- Supplementation with antioxidants and folinic acid for children with Down's syndrome: randomised controlled trial.BMJ (Clinical research ed.) · 2008Trial
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- The role of Goldilocks protein kinase DYRK1A in embryonic development.Developmental biology · 2025Review
- Cardiovascular physiology and pathophysiology in Down syndrome.Physiological research · 2022Article
- Influence of allelic differences in Down syndrome.Progress in brain research · 2020Review
- Luteolin induces hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome.Neural regeneration research · 2019Article
- Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome.Disease models & mechanisms · 2018Article
- The pattern of congenital heart defects arising from reduced Tbx5 expression is altered in a Down syndrome mouse model.BMC developmental biology · 2015Article
- Stem and progenitor cell dysfunction in human trisomies.EMBO reports · 2015Review
- Commonality in Down and fetal alcohol syndromes.Birth defects research. Part A, Clinical and molecular teratology · 2013Article
- Deficits in cognition and synaptic plasticity in a mouse model of Down syndrome ameliorated by GABAB receptor antagonists.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Genetic modifiers predisposing to congenital heart disease in the sensitized Down syndrome population.Circulation. Cardiovascular genetics · 2012Article
- The App-Runx1 region is critical for birth defects and electrocardiographic dysfunctions observed in a Down syndrome mouse model.PLoS genetics · 2012Article
- Increased efficiency of the GABAA and GABAB receptor-mediated neurotransmission in the Ts65Dn mouse model of Down syndrome.Neurobiology of disease · 2012Article
- A Sonic hedgehog (Shh) response deficit in trisomic cells may be a common denominator for multiple features of Down syndrome.Progress in brain research · 2012Review
- The use of mouse models to understand and improve cognitive deficits in Down syndrome.Disease models & mechanisms · 2011Review
- Increased survival following tumorigenesis in Ts65Dn mice that model Down syndrome.Cancer research · 2011Article
- Article
- Environmental enrichment decreases GABAergic inhibition and improves cognitive abilities, synaptic plasticity, and visual functions in a mouse model of Down syndrome.Frontiers in cellular neuroscience · 2011Article
- Cardiovascular development and survival during gestation in the Ts65Dn mouse model for Down syndrome.Anatomical record (Hoboken, N.J. : 2007) · 2011Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Since the genetic basis for Down syndrome (DS) was described, understanding the causative relationship between genes at dosage imbalance and phenotypes associated with DS has been a principal goal of researchers studying trisomy 21 (Ts21). Though inferences to the gene-phenotype relationship in humans have been made, evidence linking a specific gene or region to a particular congenital phenotype has been limited. To further understand the genetic basis for DS phenotypes, mouse models with three copies of human chromosome 21 (Hsa21) orthologs have been developed. Mouse models offer access to every tissue at each stage of development, opportunity to manipulate genetic content, and ability to precisely quantify phenotypes. Numerous approaches to recreate trisomic composition and analyze phenotypes similar to DS have resulted in diverse trisomic mouse models. A murine intraspecies comparative analysis of different genetic models of Ts21 and specific DS phenotypes reveals the complexity of trisomy and important considerations to understand the etiology of and strategies for amelioration or prevention of trisomic phenotypes. By analyzing individual phenotypes in different mouse models throughout development, such as neurologic, craniofacial, and cardiovascular abnormalities, greater insight into the gene-phenotype relationship has been demonstrated. In this review we discuss how phenotype-based comparisons between DS mouse models have been useful in analyzing the relationship of trisomy and DS phenotypes.
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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.