Pierce/Amyloid beta 42 Mouse ELISA Kit/96 tests/KMB3441

Description

TheMouseBetaAmyloid1-42(Aβ42)ELISAresearchuseonlykitistobeusedforthequantitativedeterminationofMouseandRatAβ42insamples(e.g.,cellculturesupernatants,tissuehomogenates,cerebrospinalfluid[CSF],etc.)using96-wellplatesandamicroplatereader.ThisassaywasvalidatedusingcellculturesupernatantfromaNeuro-2acellculturewhichreleasesMouseAβ42intothesurroundingmedium.TheassaywillrecognizebothnaturalandsyntheticformsofMouseandRatAβ42.Theanti-mouseAβ42antibodyusedinthiskitiscapableofselectivelydetectingAβ42andnotAβ40orAβ43.*

Performancecharacteristics
•Sensitivity:<3>
•Standardcurverange:3.12–200pg/mL
•Sampletypes:cellculturesupernatants,tissuehomogenates,cerebrospinalfluid(CSF)
•Speciescross-reactivity:mouse,rat
•Samplevolume:100μL(prediluted)
•Totalassayincubationtime:4hrs

Principleofthemethod
TheMouseAβ42kitisasolidphasesandwichEnzyme-LinkedImmunosorbentAssay(ELISA).AmonoclonalantibodytotheNH2-terminusofMouseAβhasbeencoatedontothewellsofthemicrotiterstripsprovided.Samples,includingstandardsofknownMouseAβ42content,controlspecimensandunknowns,arePipettedintothesewells.TheAβantigenbindstotheimmobilized(capture)antibody.Afterwashing,arabbitmonoclonalantibody*specificfortheCOOH-terminusofthe1-42Aβsequenceisaddedtothewells.BoundrabbitantibodyisdetectedbytheuseofahorserADIshperoxidase-labeledanti-rabbitantibody.

Afterremovalofexcessanti-rabbitantibody,asubstratesolutionisadded,whichisacteduponbytheboundenzymetoproducecolor.TheintensityofthiscoloredproductisdirectlyproportionaltotheconcentrationofMouseAβ42presentintheoriginalspecimen.

Backgroundinformation
Alzheimer’sDisease(AD)ischaracterizedbythepresenceofextracellularplaquesandintracellularneurofibrillarytangles(NFTs)inthebrain.Themajorproteincomponentoftheseplaquesisbetaamyloidpeptide(Aβ),a40to43aminoacidpeptidecleavedfromamyloidprecursorproteinbyβ-secretase(e.g.,BACE)andaputativeγ(gamma)secretase.Increasedreleaseofthe‘longerforms’ofAβpeptide,Aβ42orAβ43,whichhaveagreatertendencytoaggregatethanAβ40,occursinindividualsexpressingcertaingeneticmutations,expressingcertainApoEalleles,ormayinvolveother,stillundiscovered,factors.ManyresearcherstheorizethatitisthisincreasedreleaseofAβ42/Aβ43whichleadstotheabnormaldepositionofAβandtheassociatedneurotoxicityinthebrainsofaffectedindividuals.InpatientswithAD,reducedlevelsofAβ42inCSFhavebeendescribedaspredictiveofAD.

EachMouseAβ42ELISAkitisvalidatedforsensitivity,specificity,precision,andlot-to-lotconsistency.Seeproductinsertformoreinformationonvalidation.

Relatedlinks
LearnmoreaboutELISAkits
Learnmoreaboutotherimmunoassays

*PleaserefertotheELISAprotocolforspecificreferencecitations.