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

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 progenitors and neuroblasts. Analysis of differentiating adult Ts1Cje neural progenitors sh

SUBMITTER: Hewitt CA 

PROVIDER: S-EPMC2905390 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature