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001044126 1001_ $$0P:(DE-Juel1)201266$$aPeralta Reyes, Fernanda S.$$b0
001044126 245__ $$aLecanemab Binds to Transgenic Mouse Model‐Derived Amyloid‐β Fibril Structures Resembling Alzheimer's Disease Type I, Type II and Arctic Folds
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001044126 520__ $$aAims:Lecanemab, an Alzheimer’s disease US Food and Drug Administration-approved monoclonal antibody, was previously reported to have a high affinity against intermediately sized amyloid-β aggregates. Subsequently, it was observed by immunogold labelling that lecanemab can also bind to human type I amyloid-β fibrils. To determine whether lecanemab binds to amyloid-β fibril structures other than type I, we analysed its binding capacity to various structurally defined and pathologically relevant amyloid-β fibrils.Methods:We performed immunogold labelling with lecanemab on extracted amyloid-β fibril preparations from six different Alzheimer´s disease mouse models whose structures were previously solved by cryo-EM and quantified the relative binding affinities of lecanemab to the different fibril polymorphs.Results:Our results show that lecanemab exhibits high binding affinity to amyloid-β fibril structures that have a flexible N-terminus in common, as is the case for type I, type II and murine type III amyloid-β fibril polymorphs, which resemble or are identical to human structures observed in sporadic and familial cases of Alzheimer’s disease, including a case with the Arctic (E22G) mutation. In contrast, only weak lecanemab binding was observed for murine amyloid-β fibrils with a fixed and ordered N-terminus.Conclusions:These findings may also explain the low incidence of ARIA-E with lecanemab in clinical trials. This is because human meningeal amyloid-β fibrils derived from cerebral amyloid angiopathy affected brain tissue also contain a fixed and ordered N-terminus, most likely preventing lecanemab binding.
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001044126 7001_ $$0P:(DE-Juel1)186754$$aSommerhage, Simon$$b1
001044126 7001_ $$0P:(DE-Juel1)132029$$aWillbold, Dieter$$b2
001044126 7001_ $$0P:(DE-Juel1)132018$$aSchröder, Gunnar F.$$b3$$eCorresponding author
001044126 7001_ $$0P:(DE-Juel1)145165$$aGremer, Lothar$$b4$$eCorresponding author
001044126 773__ $$0PERI:(DE-600)2008293-9$$a10.1111/nan.70022$$gVol. 51, no. 3, p. e70022$$n3$$pe70022$$tNeuropathology & applied neurobiology$$v51$$x0305-1846$$y2025
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