Ceramide and Related-Sphingolipid Levels Are Not Altered in Disease-Associated Brain Regions of APPSL and APPSLPS1M146L Mouse Models of Alzheimers Disease Relationship with the Lack of Neurodegeneration英文文献资料.docVIP

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Ceramide and Related-Sphingolipid Levels Are Not Altered in Disease-Associated Brain Regions of APPSL and APPSLPS1M146L Mouse Models of Alzheimers Disease Relationship with the Lack of Neurodegeneration英文文献资料.doc

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Ceramide and Related-Sphingolipid Levels Are Not Altered in Disease-Associated Brain Regions of APPSL and APPSLPS1M146L Mouse Models of Alzheimers Disease Relationship with the Lack of Neurodegeneration英文文献资料

SAGE-HindawiAccesstoResearch InternationalJournalofAlzheimer’sDisease Volume2011,ArticleID920958,10pages doi:10.4061/2011/920958 ResearchArticle CeramideandRelated-SphingolipidLevelsAreNotAlteredin Disease-AssociatedBrainRegionsofAPPSLandAPPSL/PS1M146L MouseModelsofAlzheimer’sDisease:RelationshipwiththeLack ofNeurodegeneration? LaurenceBarrier,BernardFauconneau,AnastasiaNo¨el,andSabrinaIngrand GroupedeRecherchesurleVieillissementC′er′ebral,GreViCEA3808,Facult′edeM′edecineetdePharmacie,6ruedelaMil′etrie, BP199,86034PoitiersCedex,France CorrespondenceshouldbeaddressedtoLaurenceBarrier,lbarrier@univ-poitiers.fr Received27September2010;Accepted16November2010 AcademicEditor:J.Fantini Copyright?2011LaurenceBarrieretal. This is an open access article distributed under the Creative Commons Attribution License,whichpermitsunrestricteduse,distribution,andreproductioninanymedium,providedtheoriginalworkisproperly cited. There is evidence linking sphingolipid abnormalities, APP processing, and neuronal death in Alzheimer’s disease (AD). We previouslyreported astrongelevationofceramidelevelsinthebrainoftheAPP neuronal death. To extend these ?ndings, we analyzed ceramide and related-sphingolipid contents in brain from two other mousemodels(i.e.,APP andAPP )inwhichthetime-courseofpathologyisclosertothatseeninmostcurrently availablemodels.Converselytoourpreviouswork,ceramidesdidnotaccumulateindisease-associatedbrainregions(cortexand hippocampus)frombothmodels.However,theAPP /PS1Kimodelisuniqueforitsdrasticneuronallosscoincidingwithstrong accumulationofneurotoxicAβisoforms,notobservedinotheranimalmodelsofAD.Sincethereareneitherneuronallossnor SL /PS1KimousemodelofAD,preceding the SL /PS1 SL M146L SL toxicAβspeciesaccumulationinAPP SL mice,wehypothesizedthatitmightexplainthelackofceramideaccumulation,atleastin thismodel. 1.Introduction intoSMbytheadditionofphosphorylcholine.Additionally, glycosyltransferasescanattachsugartoceramide,turningit Alzheimer’s disease (A