Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from Ts1Cje and disomic C57BL/6 adult neurospheres


ABSTRACT: Down syndrome is the most common form of genetic mental retardation. How Trisomy 21 causes mental retardation remains unclear and its effects on adult neurogenesis have not been addressed. To gain insight into the mechanisms causing mental retardation we used microarrays to investigate gene expression differences between Ts1Cje (a mouse model of Down syndrome) and C57BL/6 littermate control neurospheres. The neurospheres were generated from neural stem cells and progenitors isolated from the lateral walls of the lateral ventricles from adult mice. RNA was extracted for hybridization to arrays from 3 pairs of Ts1Cje and disomic C57BL/6 littermate control 7-day old adult neurosphere cultures.

ORGANISM(S): Mus musculus

SUBMITTER: Chelsee Hewitt 

PROVIDER: E-GEOD-17760 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Gene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of Down syndrome.

Hewitt Chelsee A CA   Ling King-Hwa KH   Merson Tobias D TD   Simpson Ken M KM   Ritchie Matthew E ME   King Sarah L SL   Pritchard Melanie A MA   Smyth Gordon K GK   Thomas Tim T   Scott Hamish S HS   Voss Anne K AK  

PloS one 20100716 7


<h4>Background</h4>Down syndrome (DS) individuals suffer mental retardation with further cognitive decline and early onset Alzheimer's disease.<h4>Methodology/principal findings</h4>To understand how trisomy 21 causes these neurological abnormalities we investigated changes in gene expression networks combined with a systematic cell lineage analysis of adult neurogenesis using the Ts1Cje mouse model of DS. We demonstrated down regulation of a number of key genes involved in proliferation and cel  ...[more]

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