Soluble Gamma-secretase Modulators Attenuate Alzheimer's β-amyloid Pathology and Induce Conformational Changes in Presenilin 1.

Abstract:

:A central pathogenic event of Alzheimer's disease (AD) is the accumulation of the Aβ42 peptide, which is generated from amyloid-β precursor protein (APP) via cleavages by β- and γ-secretase. We have developed a class of soluble 2-aminothiazole γ-secretase modulators (SGSMs) that preferentially decreases Aβ42 levels. However, the effects of SGSMs in AD animals and cells expressing familial AD mutations, as well as the mechanism of γ-secretase modulation remain largely unknown. Here, a representative of this SGSM scaffold, SGSM-36, was investigated using animals and cells expressing FAD mutations. SGSM-36 preferentially reduced Aβ42 levels without affecting either α- and β-secretase processing of APP nor Notch processing. Furthermore, an allosteric site was identified within the γ-secretase complex that allowed access of SGSM-36 using cell-based, fluorescence lifetime imaging microscopy analysis. Collectively, these studies provide mechanistic insights regarding SGSMs of this class and reinforce their therapeutic potential in AD.

journal_name

EBioMedicine

journal_title

EBioMedicine

authors

Raven F,Ward JF,Zoltowska KM,Wan Y,Bylykbashi E,Miller SJ,Shen X,Choi SH,Rynearson KD,Berezovska O,Wagner SL,Tanzi RE,Zhang C

doi

10.1016/j.ebiom.2017.08.028

subject

Has Abstract

pub_date

2017-10-01 00:00:00

pages

93-101

issn

2352-3964

pii

S2352-3964(17)30345-6

journal_volume

24

pub_type

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