ArticleBehavioural brain research2011
The telomeric part of the human chromosome 21 from Cstb to Prmt2 is not necessary for the locomotor and short-term memory deficits observed in the Tc1 mouse model of Down syndrome.
Article in Behavioural brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 38 citations in OpenAlex.
- Duplication-based genetic dissection of the Down syndrome critical region reveals its complex functional organization.G3 (Bethesda, Md.) · 2026Article
- A Researcher's guide to rodent models of Down syndrome: Recent insights and translational perspectives.STAR protocols · 2026Review
- Modulation of striatal cAMP levels: A key pathway in the treatment of hyperkinetic movement disorders.iScience · 2026Article
- Alternating hemiplegia of childhood associated mutations in Atp1a3 reveal diverse neurological alterations in mice.Neurobiology of disease · 2025Article
- The COL6A5-p.Glu2272* mutation induces chronic itch in mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Kansl1 haploinsufficiency impairs autophagosome-lysosome fusion and links autophagic dysfunction with Koolen-de Vries syndrome in mice.Nature communications · 2022Article
- The HumanFrontiers in molecular neuroscience · 2022Article
- Down syndrome and Alzheimer's disease: common molecular traits beyond the amyloid precursor protein.Aging · 2020Review
- Adrenergic receptor β3 is involved in the memory consolidation process in mice.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2018Article
- Rodent models in Down syndrome research: impact and future opportunities.Disease models & mechanisms · 2017Review
- Mouse-based genetic modeling and analysis of Down syndrome.British medical bulletin · 2016Review
- Reciprocal Effects on Neurocognitive and Metabolic Phenotypes in Mouse Models of 16p11.2 Deletion and Duplication Syndromes.PLoS genetics · 2016Article
- DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome.Frontiers in behavioral neuroscience · 2016Review
- Deletion of the App-Runx1 region in mice models human partial monosomy 21.Disease models & mechanisms · 2015Article
- Opposite phenotypes of muscle strength and locomotor function in mouse models of partial trisomy and monosomy 21 for the proximal Hspa13-App region.PLoS genetics · 2015Article
- Chronic up-regulation of the SHH pathway normalizes some developmental effects of trisomy in Ts65Dn mice.Mechanisms of development · 2015Article
- Dosage of the Abcg1-U2af1 region modifies locomotor and cognitive deficits observed in the Tc1 mouse model of Down syndrome.PloS one · 2015Article
- Cognition and hippocampal plasticity in the mouse is altered by monosomy of a genomic region implicated in Down syndrome.Genetics · 2014Article
- Down syndrome: the brain in trisomic mode.Nature reviews. Neuroscience · 2012Review
- Mouse models of aneuploidy.TheScientificWorldJournal · 2012Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
Trisomy 21 or Down syndrome (DS) is the most common form of human aneuploid disorder. Increase in the copy number of human chromosome 21 genes leads to several alterations including mental retardation, heart and skeletal dysmorphologies with additional physiological defects. To better understand the genotype and phenotype relationships, several mouse models have been developed, including the transchromosomic Tc1 mouse, which carries an almost complete human chromosome 21, that displays several locomotor and cognitive alterations related to DS. In this report we explore the contribution of the genetic dosage of 47 mouse genes located in the most telomeric part of Hsa21, using a novel model, named Ms4Yah, carrying a deletion of the 2.2Mb Ctsb-Prmt2 genetic interval. We combine this deletion with the Tc1 Hsa21 in a rescue experiment. We could recapitulate most of the Tc1 phenotypes but we found no phenotypes induced by the Ms4Yah and no contribution to the Tc1-induced phenotypes even if we described new alteration in social preference but not in olfaction. Thus we conclude that the genes conserved between mouse and human, found in the most telomeric part of Hsa21, and trisomic in Tc1, are not contributing to the major Tc1 phenotypes, suggesting that the Cstb-Prmt2 region is not playing a major role in locomotor and cognitive deficits found in DS.
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