Apolipoprotein E-Mimetics Inhibit Neurodegeneration and Restore Cognitive Functions in a Transgenic Drosophila Model of Alzheimers Disease 英文参考文献.docVIP
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Apolipoprotein E-Mimetics Inhibit Neurodegeneration and Restore Cognitive Functions in a Transgenic Drosophila Model of Alzheimers Disease 英文参考文献
ApolipoproteinE-MimeticsInhibitNeurodegeneration
andRestoreCognitiveFunctionsinaTransgenic
DrosophilaModelofAlzheimer’sDisease
SvetlanaSarantseva1,SvetlanaTimoshenko1,OlgaBolshakova1,EugeniaKaraseva1,DmitryRodin1,
AlexanderL.Schwarzman1,2,MichaelP.Vitek3,4
*
1PetersburgInstituteofNuclearPhysics,RussianAcademyofSciences,Gatchina,Russia,2InstituteforExperimentalMedicine,RussianAcademyofMedicalSciences,St.
Petersburg,Russia,3DivisionofNeurology,DukeUniversityMedicalCenter,Durham,NorthCarolina,UnitedStatesofAmerica,4Cognosci,Inc.,ResearchTrianglePark,
NorthCarolina,UnitedStatesofAmerica
Abstract
Background:Mutationsoftheamyloidprecursorproteingene(APP)arefoundinfamilialformsofAlzheimer’sdisease(AD)
andsomeleadtotheelevatedproductionofamyloid-b-protein(Ab).WhileAbhasbeenimplicatedinthecausationofAD,
theexactroleplayedbyAbanditsAPPprecursorarestillunclear.
Principal Findings: In our study, Drosophila melanogaster transgenics were established as a model to analyze AD-like
pathologycausedbyAPPoverexpression.Wedemonstratedthatagerelatedchangesinthelevelsandpatternofsynaptic
proteinsaccompaniedprogressiveneurodegenerationandimpairmentofcognitivefunctionsinAPPtransgenicflies,but
that these changes may be independent from the generation of Ab. Using novel peptide mimetics of Apolipoprotein-E,
COG112orCOG133provedtobeneuroprotectiveandsignificantlyimprovedthelearningandmemoryofAPPtransgenic
flies.
Conclusions: The development of neurodegeneration and cognitive deficits was corrected by injections of COG112 or
COG133,novelmimeticsofapolipoprotein-E(apoE)withneuroprotectiveactivities.
Citation: Sarantseva S, Timoshenko S, Bolshakova O, Karaseva E, Rodin D, et al. (2009) Apolipoprotein E-Mimetics Inhibit Neurodegeneration and Restore
CognitiveFunctionsinaTransgenicDrosophilaModelofAlzheimer’sDisease.PLoSONE4(12):e8191.doi:10.1371/journal.pone.0008191
Editor:JosephElKhoury,MassachusettsGeneralHospitalandHarvardMedicalSchool,UnitedStatesofAmerica
ReceivedJune30,2009;AcceptedOctober
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