ArticleMammalian genome : official journal of the International Mammalian Genome Society2005
Identification and characterization of a new Down syndrome model, Ts[Rb(12.1716)]2Cje, resulting from a spontaneous Robertsonian fusion between T(171)65Dn and mouse chromosome 12.
Article in Mammalian genome : official journal of the International Mammalian Genome Society, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 100 citations in OpenAlex.
- Epigenetic Control of Hyperuricemia and Gout by Gene Writer DNMT1 and RNA Editor ADAR1: Mechanism of Gout and Amyloid Dissolution in Down Syndrome.Biochemical genetics · 2026Article
- Cardiopulmonary and Immune Alterations in the Ts65Dn Mouse Model of Down Syndrome and Modulation by Epigallocatechin-3-Gallate-Enriched Green Tea Extract.Pharmaceutics · 2025Article
- A Dive Into Cerebellar Dysfunction, Motor Deficits and GABAergic Signaling in Down Syndrome.Cureus · 2025Review
- Mitovesicles secreted into the extracellular space of brains with mitochondrial dysfunction impair synaptic plasticity.Molecular neurodegeneration · 2024Article
- Gene Expression Studies in Down Syndrome: What Do They Tell Us about Disease Phenotypes?International journal of molecular sciences · 2024Review
- Hippocampal CA1 Pyramidal Neurons Display Sublayer and Circuitry Dependent Degenerative Expression Profiles in Aged Female Down Syndrome Mice.Journal of Alzheimer's disease : JAD · 2024Article
- Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by TyrScience advances · 2023Article
- The Impact of Mmu17 Non-Hsa21 Orthologous Genes in the Ts65Dn Mouse Model of Down Syndrome: The Gold Standard Refuted.Biological psychiatry · 2023Article
- The Underlying Relationship between Keratoconus and Down Syndrome.International journal of molecular sciences · 2022Review
- Rodent Modeling of Alzheimer's Disease in Down Syndrome:Frontiers in neuroscience · 2022Review
- Mitochondrial Extracellular Vesicles in CNS Disorders: New Frontiers in Understanding the Neurological Disorders of the Brain.Frontiers in molecular biosciences · 2022Review
- Signalling pathways contributing to learning and memory deficits in the Ts65Dn mouse model of Down syndrome.Neuronal signaling · 2021Review
- Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules.Biomolecules · 2021Review
- Mitovesicles are a novel population of extracellular vesicles of mitochondrial origin altered in Down syndrome.Science advances · 2021Article
- Perturbation of the immune cells and prenatal neurogenesis by the triplication of the Erg gene in mouse models of Down syndrome.Brain pathology (Zurich, Switzerland) · 2020Article
- Influence of allelic differences in Down syndrome.Progress in brain research · 2020Review
- A pleiotropic role for exosomes loaded with the amyloid β precursor protein carboxyl-terminal fragments in the brain of Down syndrome patients.Neurobiology of aging · 2019Article
- Hippocampal deficits in neurodevelopmental disorders.Neurobiology of learning and memory · 2019Review
- Unbalanced dendritic inhibition of CA1 neurons drives spatial-memory deficits in the Ts2Cje Down syndrome model.Nature communications · 2019Article
- Enhanced generation of intraluminal vesicles in neuronal late endosomes in the brain of a Down syndrome mouse model with endosomal dysfunction.Developmental neurobiology · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The segmental trisomy model, Ts65Dn, has been a valuable resource for the study of the molecular and developmental processes associated with the pathogenesis of Down syndrome. However, male infertility and poor transmission of the small marker chromosome, T(17(16))65Dn, carrying the distal end of mouse Chromosome 16 (MMU16) are limiting factors in the efficient production of these animals for experimental purposes. We describe here the identification and preliminary characterization of mice, designated Ts[Rb(12.17(16))]2Cje, carrying a chromosomal rearrangement of the Ts65Dn genome whereby the marker chromosome has been translocated to Chromosome 12 (MMU12) forming a Robertsonian chromosome. This stable rearrangement confers fertility in males and increases the frequency of transmitted segmental trisomy through the female germline. We confirm retention of a dosage imbalance of human Chromosome 21 (HSA21)-homologous genes from App to the telomere and expression levels similar to Ts65Dn within the triplicated region. In addition, we characterized the dendritic morphology of granule cells in the fascia dentata in Ts[Rb(12.17(16))2Cje and 2N control mice. Quantitative confocal microscopy revealed decreased spine density on the dendrites of dentate granule cells and significantly enlarged dendritic spines affecting the entire population in Ts[Rb(12.17(16))]2Cje as compared to 2N controls. These findings document that the structural dendritic spine abnormalities are similar to those previously observed in Ts65Dn mice. We conclude that this new model of Down syndrome offers reproductive advantages without sacrificing the integrity of the Ts65Dn model.
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