dp16 mice

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  Exploring the Roots of Lung Disease in Down Syndrome

  2017 Crnic Grand Challenge Grant 50 000 "Overexpression of Anti-angiogenic Genes Impairs Lung Development in Dp16 Mice" Like this article Join Global Down Syndrome Foundation s Membership program today to receive 4 issues of the quarterly award-winning publication plus access to 4 seasonal educational Webinar Series and eligibility

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  Figures and data in Alterations of in vivo CA1 network

  2018-2-27 · A similar effect was seen using a more restrictive threshold (6 SD) even though the decrease in participation rate in Dp16 mice did not reach the significance level. Using either the more restrictive or more permissive threshold for the detection of ripples the proportion of cells plotted as a function of their participation rate in sharp

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  Frontiers Immune Dysregulation and the Increased Risk of

  The investigators reported that P(I C) administration increased circulating levels of IFN-α in WT mice and Dp16 subsequently leading to weight loss and lethal immune hypersensitivity specifically in Dp16 mice. In the lungs P(I C)-administered Dp16 mice exhibited elevated expression of IFNAR1 TLR3 and the key interferon-stimulated genes

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  P730 Poster Presentations Monday July 23 2018

  IN THE DP16 MOUSE MODEL OF DOWN SYNDROME Md. Mahiuddin Ahmed1 Athena Ching Jung Wang2 Timothy Boyd3 the Dp16 and littermate control mice post-treatment. Methods Baseline behavior assessments were started eight days before the first injection of GM-CSF or saline. Micewere injected subcutane-

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  rTg(tauP301L)4510 ALZFORUM

  2014-12-22 · T2 mice were then crossed with the CaMKIIα-tTA activator line to create bi-transgenic mice (designated rT2/T2 when homozygous for the MAPT P301L transgene). rT2/T2 mice express even more tau P301L than rTg4510 mice yet neurodegeneration is delayed and tau pathology occurs later and is less extreme in rT2/T2 mice than in rTg4510 mice. These

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  Figures and data in Alterations of in vivo CA1 network

  2018-2-27 · A similar effect was seen using a more restrictive threshold (6 SD) even though the decrease in participation rate in Dp16 mice did not reach the significance level. Using either the more restrictive or more permissive threshold for the detection of ripples the proportion of cells plotted as a function of their participation rate in sharp

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  Trisomy 21–induced dysregulation of microglial homeostasis

  2021-1-1 · We then searched for microglia-related differentially expressed genes (DEGs) encoded on chromosome 21 (mouse chromosome 16) that were associated with

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  Sleep Behavior and EEG Oscillations in Aged Dp(16)1Yey

  These results in Dp16 mice are consistent with sleep disturbances found in individuals with DS and the abnormal EEG oscillations in aged Dp16 mice suggest a potential role for GABAergic activity in these sleep and EEG abnormalities.

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  Alterations of in vivo CA1 network activity in Dp(16)1Yey

  2019-10-15 · Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models most studies have relied on in vitro measures. Here using in vivo

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  Nrf2 stabilization prevents critical oxidative damage in

  mouse embryonic fibroblasts (MEF) derived from Dp16 mice a segmentally trisomic model that reproduces several clinical pheno-types present in people with DS including cognitive impairment (Belichenko et al. 2015 Li et al. 2007 Yu et al. 2010). We found that chronic canonical Nrf2 activation is required to prevent exten-

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  Brain ventriculomegaly in Down syndrome mice is caused by

  2017-1-9 · (B–D) Dp(16)1Yey (Dp16) model mice showed a somewhat stronger phenotype. A significant part (18 out of 48) of Dp16 offspring showed abnormal morphology at 4 weeks of age with small body size associated with dome-shaped skull (D). Dissection revealed drastically enlarged cerebrum leading to aberrant positioning of the cerebellum.

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  rTg4510 Mouse Model for Alzheimer s Disease PsychoGenics

  2021-7-20 · Figure 1 Cognitive deficits in rTg4510 mice. rTg4510 mice (4 months old) show deficits in acquisition of the Morris Water Maze task (A) and spend less time in the correct quadrant during the probe test compared to either Wild type (WT) or tTA control (expressing a tetracycline-controlled transactivator (tTA) under control of the CaMKIIα promoter) mice (B).

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  Absence of Prenatal Forebrain Defects in the Dp(16)1Yey

  2016-3-9 · Dp (16)1Yey/ (hereafter called Dp16) is a recently developed mouse model of DS in which the entire region of mouse chromosome 16 that is homologous to human chromosome 21 has been triplicated. As such Dp16 mice may more closely reproduce neurodevelopmental changes occurring in humans with DS.

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  rTg(tauP301L)4510 ALZFORUM

  2014-12-22 · T2 mice were then crossed with the CaMKIIα-tTA activator line to create bi-transgenic mice (designated rT2/T2 when homozygous for the MAPT P301L transgene). rT2/T2 mice express even more tau P301L than rTg4510 mice yet neurodegeneration is delayed and tau pathology occurs later and is less extreme in rT2/T2 mice than in rTg4510 mice. These

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  Brain ventriculomegaly in Down syndrome mice is caused by

  2017-1-9 · (B–D) Dp(16)1Yey (Dp16) model mice showed a somewhat stronger phenotype. A significant part (18 out of 48) of Dp16 offspring showed abnormal morphology at 4 weeks of age with small body size associated with dome-shaped skull (D). Dissection revealed drastically enlarged cerebrum leading to aberrant positioning of the cerebellum.

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  Mouse models of Down syndrome gene content and

  2016-8-18 · Mice trisomic for all Hsa21 orthologs can be obtained by crossing the Dp10 with the Dp17 and using the double trisomic offspring to cross with the Dp16 to obtain a "triple trisomy". This breeding is time consuming and expensive.

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  Alterations of in vivo CA1 network activity in Dp(16)1Yey

  2018-2-27 · In order to investigate hippocampal spatial coding Dp(16)1Yey (Dp16 N = 6) and wild-type littermate control (WT N = 5) mice were implanted with recording electrodes in the dorsal CA1 pyramidal cell layer and allowed to explore a linear track . We observed no difference between the groups in average velocity (Dp16 4.17 ± 0.60 cm/s WT 4.57 ± 0.19 cm/s p=0.542) or total distance traveled

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  Absence of Prenatal Forebrain Defects in the Dp(16)1Yey

  2016-3-9 · Dp(16)1Yey/ (hereafter called Dp16) is a recently developed mouse model of DS in which the entire region of mouse chromosome 16 that is homologous to human chromosome 21 has been triplicated. As such Dp16 mice may more closely

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  An Integrated Human/Murine Transcriptome and Pathway

  2016-9-2 · We analyzed transcriptome data from fetuses with trisomy 21 age and -matched euploid controls and embryonic day 15.5 forebrains from Ts1Cje Ts65Dn and Dp16 mice.

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  Frontiers Down Syndrome Is a Metabolic Disease Altered

  2020-7-8 · Leptin is an inhibitor of insulin and in Ts65Dn (but also in Dp16 mice and in pancreatic islets from DS fetuses) insulin levels in plasma or secreted insulin are lower as compared to non-DS conditions. Both Ts65Dn and Dp16 models presented high plasmatic glucose levels which has been mechanistically attributed to the triplication of RCAN1.

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  Nrf2 stabilization prevents critical oxidative damage in

  mouse embryonic fibroblasts (MEF) derived from Dp16 mice a segmentally trisomic model that reproduces several clinical pheno-types present in people with DS including cognitive impairment (Belichenko et al. 2015 Li et al. 2007 Yu et al. 2010). We found that chronic canonical Nrf2 activation is required to prevent exten-

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  Oral Abstracts of the ISPD 21st International Conference

  2017-7-5 · Because Dp16 mice are trisomic for all human chromosome 21 (Hsa21) orthologues on mouse chromosome 16 (Mmu16) it may represent the best phenocopy. Ts65Dn and Ts1Cje carry a smaller number of triplicated orthologous genes yet Ts65Dn has been the most commonly used model of DS. To identify the best mouse model(s) on which to test prenatal

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  Mouse models of Down syndrome gene content and

  2016-8-18 · Down syndrome (DS) trisomy of human chromosome 21 (Hsa21) is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 of the long arm of Hsa21 but orthologs of Hsa21 genes map to segments of three mouse chromosomes Mmu16 Mmu17 and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS it is a partial trisomy currently

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  CRLF2 Overexpression Demonstrates Enhanced

  2016-12-2 · Transduced BM cells from Dp16 and wild-type (WT) control mice were co-cultured with OP9 stromal cells for one week to promote B-lymphoid lineage development and then characterized by flow cytometric Hardy fraction analysis or grown in B-lymphoid

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  Detailed evaluation of the upper airway in the Dp(16)1Yey

  2020-12-7 · Dp16 mice demonstrated craniofacial hypoplasia especially in the ventral part of the skull and the mandible and rostrally positioned hyoid. These changes were accompanied with a

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  Frontiers Down Syndrome Is a Metabolic Disease Altered

  2020-7-8 · Leptin is an inhibitor of insulin and in Ts65Dn (but also in Dp16 mice and in pancreatic islets from DS fetuses) insulin levels in plasma or secreted insulin are lower as compared to non-DS conditions. Both Ts65Dn and Dp16 models presented high plasmatic glucose levels which has been mechanistically attributed to the triplication of RCAN1.

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  Absence of Prenatal Forebrain Defects in the Dp(16)1Yey

  2016-3-4 · mental changes occurring in humans with DS. Here we present the first comprehensive cellular and behavioral study of the Dp16 forebrain from embryonic to adult stages. Unexpectedly our results demonstrate that Dp16 mice do not have prenatal brain defects

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  Mouse models of Down syndrome gene content and

  2016-8-18 · Down syndrome (DS) trisomy of human chromosome 21 (Hsa21) is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 of the long arm of Hsa21 but orthologs of Hsa21 genes map to segments of three mouse chromosomes Mmu16 Mmu17 and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS it is a partial trisomy currently

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  rTg(tauP301L)4510 ALZFORUM

  2014-12-22 · T2 mice were then crossed with the CaMKIIα-tTA activator line to create bi-transgenic mice (designated rT2/T2 when homozygous for the MAPT P301L transgene). rT2/T2 mice express even more tau P301L than rTg4510 mice yet neurodegeneration is delayed and tau pathology occurs later and is less extreme in rT2/T2 mice than in rTg4510 mice. These

• 

  Absence of Prenatal Forebrain Defects in the Dp(16)1Yey

  2016-3-4 · mental changes occurring in humans with DS. Here we present the first comprehensive cellular and behavioral study of the Dp16 forebrain from embryonic to adult stages. Unexpectedly our results demonstrate that Dp16 mice do not have prenatal brain defects

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  rTg(tauP301L)4510 ALZFORUM

  2014-12-22 · T2 mice were then crossed with the CaMKIIα-tTA activator line to create bi-transgenic mice (designated rT2/T2 when homozygous for the MAPT P301L transgene). rT2/T2 mice express even more tau P301L than rTg4510 mice yet neurodegeneration is delayed and tau pathology occurs later and is less extreme in rT2/T2 mice than in rTg4510 mice. These

• 

  Alterations of in vivo CA1 network activity in Dp(16)1Yey

  2019-10-15 · Mice engineered to model this aneuploidy exhibit Down syndrome-like memory deficits in spatial and contextual tasks. While abnormal neuronal function has been identified in these models most studies have relied on in vitro measures. Here using in vivo

• 

  Mouse models of Down syndrome gene content and

  2016-8-18 · Mice trisomic for all Hsa21 orthologs can be obtained by crossing the Dp10 with the Dp17 and using the double trisomic offspring to cross with the Dp16 to obtain a "triple trisomy". This breeding is time consuming and expensive.

• 

  Mouse models of Down syndrome gene content and

  2016-8-18 · Down syndrome (DS) trisomy of human chromosome 21 (Hsa21) is challenging to model in mice. Not only is it a contiguous gene syndrome spanning 35 of the long arm of Hsa21 but orthologs of Hsa21 genes map to segments of three mouse chromosomes Mmu16 Mmu17 and Mmu10. The Ts65Dn was the first viable segmental trisomy mouse model for DS it is a partial trisomy currently

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  JAK1 inhibition blocks lethal sterile immune responses

  2020-4-7 · Dp16 mice display lethal immune responses to IFN-inducing TLR agonists. Since Dp16 cells mount enhanced responses to IFN ligands we next investigated the response of Dp16 mice to innate immune stimuli known to trigger an IFN response.

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  Alterations of in vivo CA1 network activity in Dp(16)1Yey

  2018-2-27 · The proportion of significantly theta-modulated cells was not significantly different between Dp16 and control mice (WT 121/256 47.3 Dp16 115/259 44.4 Chi-square test p=0.514) and the firing probability of significantly theta-modulated CA1 place cells as a function of theta phase showed a highly similar pattern between the groups

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  Oral Abstracts of the ISPD 21 st International Conference

  Because Dp16 mice are trisomic for all human chromosome 21 (Hsa21) orthologues on mouse chromosome 16 (Mmu16) it may represent the best phenocopy. Ts65Dn and Ts1Cje carry a smaller number of triplicated orthologous genes yet Ts65Dn has been the most commonly used model of DS. To identify the best mouse model(s) on which to test

• 

  Mouse models of Down syndrome gene content and

  2016-8-18 · Mice trisomic for all Hsa21 orthologs can be obtained by crossing the Dp10 with the Dp17 and using the double trisomic offspring to cross with the Dp16 to obtain a "triple trisomy". This breeding is time consuming and expensive.

• 

  rTg(tauP301L)4510 ALZFORUM

  2014-12-22 · T2 mice were then crossed with the CaMKIIα-tTA activator line to create bi-transgenic mice (designated rT2/T2 when homozygous for the MAPT P301L transgene). rT2/T2 mice express even more tau P301L than rTg4510 mice yet neurodegeneration is delayed and tau pathology occurs later and is less extreme in rT2/T2 mice than in rTg4510 mice. These

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  Tau P301S (Line PS19) ALZFORUM

  2014-8-14 · Tau P301S (Line PS19) Availability The Jackson Lab Stock# 008169 Live. Research with this model is available from QPS Austria. This widely used tauopathy model was developed at the University of Pennsylvania School of Medicine by ia Lee John Trojanowski and colleagues. As first reported in 2007 on a mixed background PS19 mice

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  Brain ventriculomegaly in Down syndrome mice is caused by

  2017-1-9 · (B–D) Dp(16)1Yey (Dp16) model mice showed a somewhat stronger phenotype. A significant part (18 out of 48) of Dp16 offspring showed abnormal morphology at 4 weeks of age with small body size associated with dome-shaped skull (D). Dissection revealed drastically enlarged cerebrum leading to aberrant positioning of the cerebellum.