2012
DOI: 10.1155/2012/584071
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Mouse Models of Down Syndrome as a Tool to Unravel the Causes of Mental Disabilities

Abstract: Down syndrome (DS) is the most common genetic cause of mental disability. Based on the homology of Hsa21 and the murine chromosomes Mmu16, Mmu17 and Mmu10, several mouse models of DS have been developed. The most commonly used model, the Ts65Dn mouse, has been widely used to investigate the neural mechanisms underlying the mental disabilities seen in DS individuals. A wide array of neuromorphological alterations appears to compromise cognitive performance in trisomic mice. Enhanced inhibition due to alteration… Show more

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Cited by 160 publications
(186 citation statements)
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References 286 publications
(449 reference statements)
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“…As mentioned above, evidence for the role of DYRK1A in various DS phenotypes is partially derived from studies performed in several segmental trisomic mouse models of DS that overexpress different sets of orthologous genes of human chromosome 21 (Hsa21), including Dyrk1A (Rueda et al, 2012;Bartesaghi et al, 2011) and in transgenic mice overexpressing DYRK1A in artificial bacterial or yeast chromosomes or carrying extra copies of the corresponding murine cDNA (De la Torre et al, 2014;Ahn et al, 2006;Altafaj et al, 2001;Smith et al, 1997).…”
Section: Accepted Manuscriptmentioning
confidence: 99%
See 1 more Smart Citation
“…As mentioned above, evidence for the role of DYRK1A in various DS phenotypes is partially derived from studies performed in several segmental trisomic mouse models of DS that overexpress different sets of orthologous genes of human chromosome 21 (Hsa21), including Dyrk1A (Rueda et al, 2012;Bartesaghi et al, 2011) and in transgenic mice overexpressing DYRK1A in artificial bacterial or yeast chromosomes or carrying extra copies of the corresponding murine cDNA (De la Torre et al, 2014;Ahn et al, 2006;Altafaj et al, 2001;Smith et al, 1997).…”
Section: Accepted Manuscriptmentioning
confidence: 99%
“…TS mice replicate many DS-like abnormalities, including alterations in behavior, learning and memory, brain morphology and hypocellularity, neurogenesis, neuronal connectivity and electrophysiological and neurochemical processes (Rueda et al, 2012;Bartesaghi et al, 2011). Similar to DS individuals, the TS mouse also shows age-dependent cognitive decline and degeneration starting at the age of 6 months, including cholinergic and noradrenergic neuron degeneration, increases in the levels of APP protein and Aβ peptides and tau hyperphosphorylation (Millan Sanchez et al, 2012;Rueda et al, 2010;Netzer et al, 2010;Liu et al, 2008;Seo et al, 2005).…”
Section: Accepted Manuscriptmentioning
confidence: 99%
“…This model is segmentally trisomic for a portion of the mouse chromosome 16 that is orthologous to the long arm of the human chromosome 21. This segment contains approximately 140 genes, many of which are highly conserved between mice and humans [2][3][4]. These mice display delay in the acquisition of a number of sensory and motor tasks [5,6], as well as defects in learning and in the execution of memory tasks mediated by the hippocampus [5,[7][8][9][10][11][12][13], and deficits in long-term potentiation (LTP) [14][15][16].…”
Section: Introductionmentioning
confidence: 99%
“…Recent analyses showed a heterozygous deletion on Mmu12 in Ts1Cje mice, which is not syntenic to Hsa21. 13,16 The phenotypes of Ts65Dn and Ts1Cje mice have been extensively characterized and, although these mice are not perfect molecular mimics of human DS, they do show many phenotypic features of the human syndrome [17][18][19][20][21] (Supplementary Table S2). …”
Section: Modeling Ds At the Early Stagementioning
confidence: 99%