Early Functional Deficit and Microglial Disturbances in a Mouse Model of Amyotrophic Lateral Sclerosis 英文参考文献.docVIP

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Early Functional Deficit and Microglial Disturbances in a Mouse Model of Amyotrophic Lateral Sclerosis 英文参考文献.doc

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Early Functional Deficit and Microglial Disturbances in a Mouse Model of Amyotrophic Lateral Sclerosis 英文参考文献

EarlyFunctionalDeficitandMicroglialDisturbancesina MouseModelofAmyotrophicLateralSclerosis YannickNicolasGerber1,2.,Jean-CharlesSabourin3.,MiriamRabano4,MariadMVivanco4 ,Florence EvelynePerrin1,2,3 * 1INSERM U1051, Institute for Neurosciences of Montpellier, Pathophysiology and Therapy of Sensory and Motor Deficits, Saint Elio Hospital, Montpellier, France, 2IKERBASQUEBasqueFoundationforScience,Bilbao,Spain,3IntegrativeBiologyofNeurodegeneration,NeuroscienceDepartment,UniversityoftheBasqueCountry, Leioa,Spain,4CICbioGUNE,CellBiologyStemCellsUnit,TechnologicalParkofBizkaia,Derio,Spain Abstract Background:Amyotrophiclateralsclerosis(ALS)isaneurodegenerativedisordercharacterizedbyselectivemotoneurons degeneration.There istoday noclear-cut pathogenesissequencenoranytreatment.Howevergrowingevidences arein favor of the involvement, besides neurons, of several partners such as glia andmuscles. To better characterize the time courseofpathologicaleventsinananimalmodelthatrecapitulateshumanALSsymptoms,weinvestigatedfunctionaland cellularcharacteristicsofhSOD1G93A mice. MethodsandFindings:WehaveevaluatedlocomotorfunctionofhSOD1G93Amicethroughdynamicwalkingpatternsand spontaneousmotoractivityanalysis.Wedetectedearlyfunctionaldeficitsthatredefinesymptomsonsetat60daysofage, i.e.20daysearlierthanpreviouslydescribed.Moreover,sequentialcombinationoftheseapproachesallowsmonitoringof motoractivityuptodiseaseendstage.Totentativelycorrelateearlyfunctionaldeficitwithcellularalterationswehaveused flowcytometryandimmunohistochemistryapproachestocharacterizeneuromuscularjunctions,astrocytesandmicroglia. Weshowthat(1)decreaseinneuromuscularjunction’snumbercorrelateswithmotorimpairment,(2)astrocytesnumberis notalteredatpre-andearly-symptomaticagesbutintraspinalrepartitionismodifiedatsymptomsonset,and(3)microglia modificationsprecedediseaseonset.Atpre-symptomaticage,weshowadecreaseinmicroglianumberwhereasatonsetof thediseasetwodistinctmicrogliasub-populationsemerge. Conclusions: In conclus