Journal article
Gene network disruptions and neurogenesis defects in the adult Ts1Cje mouse model of down syndrome
CA Hewitt, KH Ling, TD Merson, KM Simpson, ME Ritchie, SL King, MA Pritchard, GK Smyth, T Thomas, HS Scott, AK Voss
Plos One | Published : 2010
Abstract
Background: Down syndrome (DS) individuals suffer mental retardation with further cognitive decline and early onset Alzheimer's disease. Methodology/Principal Findings: 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 cell cycle progression including Mcm7, Brca2, Prim1, Cenpo and Aurka in trisomic neurospheres. We found that trisomy did not affect the number of adult neural stem cells but resulted in reduced numbers of neural prog..
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Awarded by National Health and Medical Research Council
Funding Acknowledgements
This work was supported by the APEX Foundation for Research into Intellectual Disability Limited to C. H.; National Health and Medical Research Council fellowships 171601 and 461204 to H. S. S. and 575512 to A. K. V.; National Health and Medical Research Council Grants 219176, 257501 and 257529 to H. S. S. and G. K. S. K.-H. L. was a recipient of Melbourne International Fee Remission Scholarship (MIFRS) and Universiti Putra Malaysia Staff Training Scholarship (UPMSTS), and an Adelaide Fee Scholarship International (AFSI) equivalent award. The microarrays were performed by the Australian Genome Research Facility, which was established through the Commonwealth-funded Major National Research Facilities program. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.