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Maternal choline supplementation improves spatial learning and adult hippocampal neurogenesis in the Ts65Dn mouse model of Down syndrome

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Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome

Aziz, N. M., Guedj, F., Pennings, J. L. A., Olmos-Serrano, J. L., Siegel, A., Haydar, T. F., & Bianchi, D. W. (2018) · Disease Models &amp; Mechanisms · doi:10.1242/dmm.031013 · Cited by 118 · see citing works

Mitochondrial dysfunction and tau hyperphosphorylation in Ts1Cje, a mouse model for Down syndrome

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Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current

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The “gene dosage effect” hypothesis versus the “amplified developmental instability” hypothesis in Down syndrome

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APP-dependent up-regulation of Ptch1 underlies proliferation impairment of neural precursors in Down syndrome

Trazzi, S., Mitrugno, V. M., Valli, E., Fuchs, C., Rizzi, S., Guidi, S., Perini, G., Bartesaghi, R., & Ciani, E. (2011) · Human Molecular Genetics · doi:10.1093/hmg/ddr033 · Cited by 112 · see citing works

Abnormal synaptic plasticity in the Ts1Cje segmental trisomy 16 mouse model of Down syndrome

Siarey, R. J., Villar, A. J., Epstein, C. J., & Galdzicki, Z. (2005) · Neuropharmacology · doi:10.1016/j.neuropharm.2005.02.012 · Cited by 112 · see citing works

Genetic dissection of Down syndrome-associated congenital heart defects using a new mouse mapping panel

Lana‐Elola, E., Watson-Scales, S., Slender, A., Gibbins, D., Martineau, A., Douglas, C., Mohun, T. J., Fisher, E., & Tybulewicz, V. L. J. (2016) · eLife · doi:10.7554/elife.11614 · Cited by 105 · see citing works

Mental retardation in Down syndrome: From gene dosage imbalance to molecular and cellular mechanisms

Rachidi, M., & Lopes, C. (2007) · Neuroscience Research · doi:10.1016/j.neures.2007.08.007 · Cited by 111 · see citing works

Enlarged Brain Ventricles and Impaired Neurogenesis in the Ts1Cje and Ts2Cje Mouse Models of Down Syndrome

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GABAergic neurotransmission and new strategies of neuromodulation to compensate synaptic dysfunction in early stages of Alzheimer’s disease

Nava-Mesa, M. O., Jiménez‐Díaz, L., Yajeya, J., & Navarro‐López, J. D. (2014) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2014.00167 · Cited by 105 · see citing works

Estrogen restores cognition and cholinergic phenotype in an animal model of Down syndrome

Granholm, A., Ford, K. A., Hyde, L. A., Bimonte, H. A., Hunter, C. L., NELSON, M., Albeck, D. S., Sanders, L., Mufson, E. J., & Crnic, L. S. (2002) · Physiology & Behavior · doi:10.1016/s0031-9384(02)00884-3 · Cited by 104 · see citing works

Mice trisomic for a bacterial artificial chromosome with the single-minded 2 gene (Sim2) show phenotypes similar to some of those present in the partial trisomy 16 mouse models of Down syndrome

Chrast, R. (2000) · Human Molecular Genetics · doi:10.1093/hmg/9.12.1853 · Cited by 102 · see citing works

Mental retardation and associated neurological dysfunctions in Down syndrome: A consequence of dysregulation in critical chromosome 21 genes and associated molecular pathways

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Deregulated mTOR-mediated translation in intellectual disability.

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From Down Syndrome to the “Human” in “Human Genetics”**Previously presented at the annual meeting of The American Society of Human Genetics, in San Diego, on October 15, 2001.

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The use of mouse models to understand and improve cognitive deficits in Down syndrome

Das, I., & Reeves, R. H. (2011) · Disease Models & Mechanisms · doi:10.1242/dmm.007716 · Cited by 99 · see citing works

The Mouse Brain Transcriptome by SAGE: Differences in Gene Expression between P30 Brains of the Partial Trisomy 16 Mouse Model of Down Syndrome (Ts65Dn) and NormalsPreprint

Chrast, R., Scott, H. S., Papasavvas, M. P., Rossier, C., Antonarakis, E. S., Barras, C., Davisson, M. T., Schmidt, C., Estivill, X., Dierssen, M., et al. (2000) · Genome Research · doi:10.1101/gr.10.12.2006 · Cited by 100 · see citing works

Understanding mental retardation in Down's syndrome using trisomy 16 mouse models

Galdzicki, Z., & Siarey, R. J. (2003) · Genes Brain & Behavior · doi:10.1034/j.1601-183x.2003.00024.x · Cited by 98 · see citing works

Preservation of long-term memory and synaptic plasticity despite short-term impairments in the Tc1 mouse model of Down syndromePreprint

Morice, É., Andreae, L. C., Cooke, S. F., Vanes, L., Fisher, E., Tybulewicz, V. L. J., & Bliss, T. (2008) · Learning & Memory · doi:10.1101/lm.969608 · Cited by 97 · see citing works

Identification and characterization of a new Down syndrome model, Ts[Rb(12.1716)]2Cje, resulting from a spontaneous Robertsonian fusion between T(1716)65Dn and mouseChromosome 12

Villar, A. J., Belichenko, P. V., Gillespie, A. M., Kozy, H. M., Mobley, W. C., & Epstein, C. J. (2005) · Mammalian Genome · doi:10.1007/s00335-004-2428-7 · Cited by 96 · see citing works

Heterotrisomy, a significant contributing factor to ventricular septal defect associated with Down syndrome?

Baptista, M. J., Fairbrother, U. L., Howard, C., Farrer, M. J., Davies, G. E., Trikka, D., Maratou, K., Redington, A. N., Greve, G., Njølstad, P. R., et al. (2000) · Human Genetics · doi:10.1007/s004390000395 · Cited by 95 · see citing works

Aneuploidy in the normal and diseased brain

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Impairments in motor coordination without major changes in cerebellar plasticity in the Tc1 mouse model of Down syndrome

Galante, M., Jani, H., Vanes, L., Daniel, H., Fisher, E., Tybulewicz, V. L. J., Bliss, T. V. P., & Morice, É. (2009) · Human Molecular Genetics · doi:10.1093/hmg/ddp055 · Cited by 89 · see citing works

NMDA-Mediated Regulation of DSCAM Dendritic Local Translation Is Lost in a Mouse Model of Down's Syndrome

Alves-Sampaio, A., Troca-Marín, J. A., & Montesinos, M. L. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3457-10.2010 · Cited by 86 · see citing works

Two key genes closely implicated with the neuropathological characteristics in Down syndrome: DYRK1A and RCAN1

Park, J., Oh, Y., & Chung, K. C. (2009) · BMB Reports · doi:10.5483/bmbrep.2009.42.1.006 · Cited by 86 · see citing works

The cerebellar transcriptome during postnatal development of the Ts1Cje mouse, a segmental trisomy model for Down syndrome

Dauphinot, L., Lyle, R., Rivals, I., Dang, M., Moldrich, R. X., Golfier, G., Ettwiller, L. M., Toyama, K., Rossier, J., Personnaz, L., et al. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddi033 · Cited by 86 · see citing works

Hippocampal deficits in neurodevelopmental disorders

Li, Y., Shen, M., Stockton, M. E., & Zhao, X. (2018) · Neurobiology of Learning and Memory · doi:10.1016/j.nlm.2018.10.001 · Cited by 84 · see citing works

Down syndrome cell adhesion molecule DSCAM mediates homophilic intercellular adhesion

Agarwala, K. L., Nakamura, S., Tsutsumi, Y., & Yamakawa, K. (2000) · Molecular Brain Research · doi:10.1016/s0169-328x(00)00108-x · Cited by 83 · see citing works

Mild Impairment of Learning and Memory in Mice Overexpressing the mSim2 Gene Located on Chromosome 16: An Animal Model of Down's Syndrome

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Abnormal expression of the G‐protein‐activated inwardly rectifying potassium channel 2 (GIRK2) in hippocampus, frontal cortex, and substantia nigra of Ts65Dn mouse: A model of Down syndrome

Harashima, C., Jacobowitz, D. M., Witta, J., Borke, R. C., Best, T. K., Siarey, R. J., & Galdzicki, Z. (2005) · The Journal of Comparative Neurology · doi:10.1002/cne.20844 · Cited by 82 · see citing works

On the cause of mental retardation in Down syndrome: extrapolation from full and segmental trisomy 16 mouse models

Galdzicki, Z., Siarey, R. J., Pearce, R., Stoll, J., & Rapoport, S. I. (2001) · Brain Research Reviews · doi:10.1016/s0926-6410(00)00074-4 · Cited by 81 · see citing works

Impact of brain-behavior phenotypying of genetically-engineered mice on research of neuropsychiatric disorders

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The complex SNP and CNV genetic architecture of the increased risk of congenital heart defects in Down syndromePreprint

Sailani, M. R., Makrythanasis, P., Valsesia, A., Santoni, F. A., Deutsch, S., Popadin, K. Y., Borel, C., Migliavacca, E., Sharp, A. J., Saïl, G. D., et al. (2013) · Genome Research · doi:10.1101/gr.147991.112 · Cited by 82 · see citing works

Behavioral validation of the Ts65Dn mouse model for Down syndrome of a genetic background free of the retinal degeneration mutation Pde6brd1

Costa, A. C. S., Stasko, M. R., Schmidt, C., & Davisson, M. T. (2009) · Behavioural Brain Research · doi:10.1016/j.bbr.2009.08.034 · Cited by 80 · see citing works

Prospects for Improving Brain Function in Individuals with Down Syndrome

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Transcriptional consequences of autosomal trisomy: primary gene dosage with complex downstream effects

FitzPatrick, D. R. (2005) · Trends in Genetics · doi:10.1016/j.tig.2005.02.012 · Cited by 80 · see citing works

Dyrk1a from gene function in development and physiology to dosage correction across life span in down syndrome

Atas-Ozcan, H., Brault, V., Duchon, A., & Herault, Y. (2021) · Genes · doi:10.3390/genes12111833 · Cited by 78 · see citing works

Altered signaling pathways underlying abnormal hippocampal synaptic plasticity in the Ts65Dn mouse model of Down syndrome

Siarey, R. J., Kline‐Burgess, A., Cho, M., Balbo, A., Best, T. K., Harashima, C., Klann, E., & Galdzicki, Z. (2006) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2006.03971.x · Cited by 86 · see citing works

Trisomy of the G protein-coupled K + channel gene, Kcnj6 , affects reward mechanisms, cognitive functions, and synaptic plasticity in mice

Cooper, A., Grigoryan, G., Guy-David, L., Tsoory, M., Chen, A., & Reuveny, E. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1109099109 · Cited by 76 · see citing works

Is it possible to improve neurodevelopmental abnormalities in Down syndrome?

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Differential effects of trisomy on brain shape and volume in related aneuploid mouse models

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Genetic Dissection of Region Associated with Behavioral Abnormalities in Mouse Models for Down Syndrome

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A behavioral assessment of Ts65Dn mice: a putative Down syndrome model

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Ts1Cje mouse model for Down syndrome research

Ling, K. H. (2015) · Universiti Putra Malaysia Institutional Repository (Universiti Putra Malaysia)

A mouse model for Down syndrome exhibits learning and behaviour deficits [see comments]

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Ts1Cje Down syndrome model mice exhibit environmental stimuli-triggered locomotor hyperactivity and sociability concurrent with increased flux through central dopamine and serotonin metabolism

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