Gene Network Disruptions and Neurogenesis Defects in the Adult Ts1Cje Mouse Model of Down Syndrome 英文参考文献.docVIP

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2017-05-11 发布于上海
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Gene Network Disruptions and Neurogenesis Defects in the Adult Ts1Cje Mouse Model of Down Syndrome 英文参考文献.doc

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Gene Network Disruptions and Neurogenesis Defects in the Adult Ts1Cje Mouse Model of Down Syndrome 英文参考文献

GeneNetworkDisruptionsandNeurogenesisDefectsin theAdultTs1CjeMouseModelofDownSyndrome ChelseeA.Hewitt1,3*,King-HwaLing1,4,6,TobiasD.Merson1,KenM.Simpson1,MatthewE.Ritchie1, SarahL.King1,MelanieA.Pritchard5,GordonK.Smyth1,TimThomas1,2,HamishS.Scott1,4*.,AnneK. Voss1,2. 1The Walter and Eliza Hall Institute of Medical Research, Melbourne, Australia, 2Department of Medical Biology, University of Melbourne, Melbourne, Australia, 3DepartmentofPathology,ThePeterMacCallumCancerCentre,Melbourne,Australia,4DepartmentofMolecularPathology,TheCentreforCancerBiology,TheInstitute of Medical and Veterinary Science and The Hanson Institute, SA Pathology, and The Adelaide Cancer Research Institute, School of Medicine, University of Adelaide, Adelaide,Australia,5DepartmentofBiochemistryandMolecularBiology,MonashUniversity,Victoria,Australia,6DepartmentofObstetricsandGynaecology,Facultyof MedicineandHealthSciences,UniversitiPutraMalaysia,Selangor,Malaysia Abstract Background: Down syndrome (DS) individuals suffer mental retardation with further cognitive decline and early onset Alzheimer’sdisease. Methodology/PrincipalFindings:Tounderstandhowtrisomy21causestheseneurologicalabnormalitiesweinvestigated changes in gene expression networks combined with a systematic cell lineage analysis of adult neurogenesis using the Ts1CjemousemodelofDS.Wedemonstrateddownregulationofanumberofkeygenesinvolvedinproliferationandcell cycleprogressionincludingMcm7,Brca2,Prim1,CenpoandAurkaintrisomicneurospheres.Wefoundthattrisomydidnot affect the number of adult neural stem cells but resulted in reduced numbers of neural progenitors and neuroblasts. AnalysisofdifferentiatingadultTs1Cjeneuralprogenitorsshowedaseverereductioninnumbersofneuronsproducedwith atendencyforlesselaborateneurites,whilstthenumbersofastrocyteswasincreased. Conclusions/Significance:Wehaveshownthattrisomyaffectsanumberofelementsofadultneurogenesislikelytoresult in a progressive pathogenesis and consequently providing the potential for the