scholarly journals 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 Normals

2000 ◽  
Vol 10 (12) ◽  
pp. 2006-2021 ◽  
Author(s):  
R. Chrast
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Model ◽  
Mouse Brain ◽  
Partial Trisomy ◽  
Trisomy 16 ◽  
Brain Transcriptome

scholarly journals 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 Normals

2000 ◽  
Vol 10 (12) ◽  
pp. 2006-2021 ◽  
Author(s):  
Roman Chrast ◽  
Hamish S. Scott ◽  
Marie Pierre Papasavvas ◽  
Colette Rossier ◽  
Emmanuel S. Antonarakis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Brain ◽  
Expression Profiles ◽  
System Structure ◽  
Abnormal Development ◽  
Mammalian Brain ◽  
Normal Male ◽  
Normal Female ◽  
Brain Transcriptome

Trisomy 21, or Down syndrome (DS), is the most common genetic cause of mental retardation. Changes in the neuropathology, neurochemistry, neurophysiology, and neuropharmacology of DS patients' brains indicate that there is probably abnormal development and maintenance of central nervous system structure and function. The segmental trisomy mouse (Ts65Dn) is a model of DS that shows analogous neurobehavioral defects. We have studied the global gene expression profiles of normal and Ts65Dn male and normal female mice brains (P30) using the serial analysis of gene expression (SAGE) technique. From the combined sample we collected a total of 152,791 RNA tags and observed 45,856 unique tags in the mouse brain transcriptome. There are 14 ribosomal protein genes (nine underexpressed) among the 330 statistically significant differences between normal male and Ts65Dn male brains, which possibly implies abnormal ribosomal biogenesis in the development and maintenance of DS phenotypes. This study contributes to the establishment of a mouse brain transcriptome and provides the first overall analysis of the differences in gene expression in aneuploid versus normal mammalian brain cells.

scholarly journals Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities

1998 ◽  
Vol 95 (11) ◽  
pp. 6256-6261 ◽  
Author(s):  
H. Sago ◽  
E. J. Carlson ◽  
D. J. Smith ◽  
J. Kilbridge ◽  
E. M. Rubin ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Partial Trisomy ◽  
Trisomy 16 ◽  
Behavioral Abnormalities

scholarly journals Consequences of Trisomy 16 for Mouse Brain Development: Corticogenesis in a Model of Down Syndrome

1996 ◽  
Vol 16 (19) ◽  
pp. 6175-6182 ◽  
Author(s):  
Tarik F. Haydar ◽  
Mary E. Blue ◽  
Mark E. Molliver ◽  
Bruce K. Krueger ◽  
Paul J. Yarowsky
Keyword(s):  
Down Syndrome ◽  
Brain Development ◽  
Mouse Brain ◽  
Trisomy 16 ◽  
Mouse Brain Development

scholarly journals Gene expression signature of cerebellar hypoplasia in a mouse model of Down syndrome during postnatal development

BMC Genomics ◽  
2009 ◽  
Vol 10 (1) ◽  
pp. 138 ◽  
Author(s):  
Julien Laffaire ◽  
Isabelle Rivals ◽  
Luce Dauphinot ◽  
Fabien Pasteau ◽  
Rosine Wehrle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Model ◽  
Postnatal Development ◽  
Gene Expression Signature ◽  
Cerebellar Hypoplasia ◽  
Expression Signature

scholarly journals Gene Expression Profiling in a Mouse Model Identifies Fetal Liver- and Placenta-Derived Potential Biomarkers for Down Syndrome Screening

PLoS ONE ◽  
2011 ◽  
Vol 6 (4) ◽  
pp. e18866 ◽  
Author(s):  
Jeroen L. A. Pennings ◽  
Wendy Rodenburg ◽  
Sandra Imholz ◽  
Maria P. H. Koster ◽  
Conny T. M. van Oostrom ◽  
...  
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Model ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Fetal Liver ◽  
Potential Biomarkers ◽  
Down Syndrome Screening

scholarly journals Maternal Choline Supplementation Alters Basal Forebrain Cholinergic Neuron Gene Expression in the Ts65Dn Mouse Model of Down Syndrome

2019 ◽  
Vol 79 (7) ◽  
pp. 664-683 ◽  
Author(s):  
Christy M. Kelley ◽  
Stephen D. Ginsberg ◽  
Melissa J. Alldred ◽  
Barbara J. Strupp ◽  
Elliott J. Mufson
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Model ◽  
Basal Forebrain ◽  
Cholinergic Neuron ◽  
Ts65dn Mouse ◽  
Basal Forebrain Cholinergic Neuron

scholarly journals The fetal brain transcriptome and neonatal behavioral phenotype in the Ts1Cje mouse model of Down syndrome

2015 ◽  
Vol 167 (9) ◽  
pp. 1993-2008 ◽  
Author(s):  
Faycal Guedj ◽  
Jeroen L. A. Pennings ◽  
Millie A. Ferres ◽  
Leah C. Graham ◽  
Heather C. Wick ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Fetal Brain ◽  
Behavioral Phenotype ◽  
Brain Transcriptome

Gene expression variation in three brain tissues of a mouse model of down syndrome

2005 ◽  
Vol 2005 (Fall) ◽  
Author(s):  
Marc Sultan ◽  
Daniela Balzereit ◽  
Nidhi G Saran ◽  
Simone Guenther ◽  
Karl Guegler ◽  
...  
Keyword(s):  
Gene Expression ◽  
Down Syndrome ◽  
Mouse Model ◽  
Gene Expression Variation ◽  
Expression Variation ◽  
Brain Tissues

scholarly journals Assessing the requirements of prenatal UBE3A expression for rescue of behavioral phenotypes in a mouse model for Angelman syndrome

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Monica Sonzogni ◽  
Peipei Zhai ◽  
Edwin J. Mientjes ◽  
Geeske M. van Woerden ◽  
Ype Elgersma
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Brain Development ◽  
Mouse Brain ◽  
Angelman Syndrome ◽  
Neurodevelopmental Disorder ◽  
Brain Regions ◽  
Critical Function ◽  
Behavioral Phenotypes ◽  
Mouse Brain Development

Abstract Background Angelman syndrome (AS) is a rare neurodevelopmental disorder caused by the loss of functional ubiquitin protein ligase E3A (UBE3A). In neurons, UBE3A expression is tightly regulated by a mechanism of imprinting which suppresses the expression of the paternal UBE3A allele. Promising treatment strategies for AS are directed at activating paternal UBE3A gene expression. However, for such strategies to be successful, it is important to know when such a treatment should start, and how much UBE3A expression is needed for normal embryonic brain development. Methods Using a conditional mouse model of AS, we further delineated the critical period for UBE3A expression during early brain development. Ube3a gene expression was induced around the second week of gestation and mouse phenotypes were assessed using a behavioral test battery. To investigate the requirements of embryonic UBE3A expression, we made use of mice in which the paternal Ube3a allele was deleted. Results We observed a full behavioral rescue of the AS mouse model phenotypes when Ube3a gene reactivation was induced around the start of the last week of mouse embryonic development. We found that full silencing of the paternal Ube3a allele was not completed till the first week after birth but that deletion of the paternal Ube3a allele had no significant effect on the assessed phenotypes. Limitations Direct translation to human is limited, as we do not precisely know how human and mouse brain development aligns over gestational time. Moreover, many of the assessed phenotypes have limited translational value, as the underlying brain regions involved in these tasks are largely unknown. Conclusions Our findings provide further important insights in the requirement of UBE3A expression during brain development. We found that loss of up to 50% of UBE3A protein during prenatal mouse brain development does not significantly impact the assessed mouse behavioral phenotypes. Together with previous findings, our results indicate that the most critical function for mouse UBE3A lies in the early postnatal period between birth and P21.

scholarly journals AppGene Dosage Modulates Endosomal Abnormalities of Alzheimer's Disease in a Segmental Trisomy 16 Mouse Model of Down Syndrome

2003 ◽  
Vol 23 (17) ◽  
pp. 6788-6792 ◽  
Author(s):  
Anne M. Cataldo ◽  
Suzana Petanceska ◽  
Corrinne M. Peterhoff ◽  
Nicole B. Terio ◽  
Charles J. Epstein ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Down Syndrome ◽  
Mouse Model ◽  
Trisomy 16
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