科普

　　标题：Boostingthebrainswastedisposalsystem
　　作者：CHARITUNIVERSITTSMEDIZINBERLIN
　　原文链接：http：www。eurekalert。orgpubreleases201510cubbtb101315。php
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　　IMAGE：LEFT：APLAQUES（GREEN）SURROUNDEDBYRESIDENTMICROGLIA（BLUE）INADMOUSEBRAINS。RIGHT：NEWPERIPHERALMACROPHAGES（BLUE）THATMIGRATEDINTOTHEBRAINOFADMICEUPONABLATIONOFRESIDENT。。。
　　Worldwide，morethan20ofpersonsovertheageof85sufferfromAlzheimersdisease（AD）。Depositsofbetaamyloid（A）peptiderepresentanimportanttargetforresearchintoAD。Thesepeptidefragments，whichaccumulateinthebrainsofADpatients，playanimportantroleinthepathogenesisofAD。AresearchteamheadedbyProf。Dr。FrankHeppner，DirectorofCharitsDepartmentofNeuropathology，hadpreviouslydemonstratedthatthebrainsimmunecells，knownasmicroglia，areimpairedinthecourseofAD。，Thus，microgliainADareunabletofulfilltheirprimarypurpose，whichistheeliminationofforeignsubstancesorabnormalstructuressuchaspathologicalbetaamyloidpeptides。
　　Inthiscurrentstudy，thesameteamofresearcherssetouttoinvestigatewhetheritmightbepossibletopromptmacrophages，theperipheralcounterpartsofmicrogliathatresideoutsidethebrainandintheblood，tomigratetothebrain，inordertotakeoverroleofthedysfunctionalmicroglia。TheresearchersstartedbydevelopingamousemodelofAD，inwhichtheyablatedmicroglia。Thiscreatedanemergencysituation，whichpromptedthebraintoinitiateaninfiltrationresponse，andresultedinbloodbornemacrophagesmigratingfromperipheralsitestorepopulatethebrain。Theseperipheralderivedcellssubsequentlyunderwentfurtherdevelopmentinthebrainthatrenderedthemsimilartomicroglia，however，withoutimpactingADpathologyand，ratherthanclusteringaroundAdeposits，theycompletelyignoredtheirpresence。Thesefindingsaremirroredbyanotherstudy，whichwasconductedbyagroupofresearchersfromtheUniversityofTbingen，andalsopublishedinthecurrentvolumeoftheJournalofExperimentalMedicine。
　　Prof。Dr。FrankHeppnerexplainsthatinordertomaketheseperipheralmacrophagesinterestedinApeptides，ADmiceharboringbloodbornemacrophagesinsteadofresidentmicrogliainthebrainweregivenanAvaccineanapproachthatiscurrentlybeinginvestigatedinseveralclinicaltrials，andremainsthesubjectofintensediscussion。However，eventhisadditionalstimulationdidnotrendertheseperipheralmacrophagesanymoreeffectivethanthebrainsresidentmicroglia。Obviously，motivatingresidentmicrogliaorperipheralmacrophagestorealizetheirfullpotentialwillrequireadifferent，oradditional，stimulus，saysProf。Heppner。However，ourdataisofrelevance，insofarasmanyrecentstudieshaveidentifiedmicrogliaasacrucialplayerinboththedevelopmentandprogressionofAlzheimersdisease。Itisthereforeoffundamentalimportance，notleastinrelationtothedevelopmentofnewtreatmentoptions，thatweshouldgainadetailedinsightintoboththeroleandfunctionofmicrogliaandmacrophagesinAD。
　　Theresearchersarenowplanningtoconductfurtherstudiesaimedatidentifyingthemissingstimulus。Bydoingso，theyhopetoensurethatthephagocyticcellsinquestioncanreturntofulfillingtheiroriginalfunction。