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Kinetic fingerprints differentiate anti-Aβ therapies

biorxiv. 2020; 
Sara Linse,  Tom Scheidt,  Katja Bernfur,  Michele Vendruscolo,  Christopher M. Dobson,  Samuel I. A. Cohen,  Eimantas Sileikis,  Martin Lundquist,  Fang Qian,  Tiernan O’Malley,  Thierry Bussiere,  Paul H. Weinreb,  Catherine K. Xu,  Georg Meisl,  Sean R. A. Devenish,  Tuomas P. J. Knowles,  Oskar Hansson
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Molecular Biology Reagents EDDIE-Aβ1-42 with the amino acid sequence MELNHFELLYKTSKQKPVGVEEPVYDTAGRPLFGNPSEVHPQSTLKLPHDRGEDDIETT LRDLPRKGDCRSGNHLGPVSGIYIKPGPVYYQDYTGPVYHRAPLEFFDETQFEETTKRIG RVTGSDGKLYHIYVEVDGEILLKQAKRGTPRTLKWTRNTTNCPLWVTSCDAEFRHDSG YEVHHQKLVFFAEDVGSNKGAIIGLMVGGVVIA, with the Aβ1-42 sequence underlined, was expressed from a Pet3a plasmid (purchased from Genscript, Piscataway, New Jersey) in E. coli BL21 DE3 PlysS star in overnight express medium (2.5 mM Na2HPO4, 2.5 mM KH2PO4, 12 mM (NH4)2SO4, 1 mM MgSO4, 0.1 g/L glucose, 0.4 g/L lactose, 1 g/L glycerol, 10 g/L NaCl, 10 g/L tryptone, 5 g/L Bacto yeast extract, 50 mg/L ampicillin, 30 mg/L chloramphenicol). Get A Quote

摘要

The amyloid cascade hypothesis, according to which the self-assembly of amyloid-β peptide (Aβ) is a causative process in Alzheimer’s disease, has driven many therapeutic efforts for the past 20 years. Failures of clinical trials investigating Aβ-targeted therapies have been interpreted as evidence against this hypothesis, irrespective of the characteristics and mechanisms of action of the therapeutic agents, which are highly challenging to assess. We bring together kinetic analysis with quantitative binding measurements to address the mechanisms of action of four clinical stage anti-Aβ antibodies, aducanumab, gantenerumab, bapineuzumab and solanezumab. We reveal and quantify the striking differences of th... More

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