A Newly Designed Molecule J2326 for Alzheimer's Disease Disaggregates Amyloid Fibrils and Induces Neurite Outgrowth

Chang P, et al., 92:146-57, Neuropharmacology, 2015

This study has focused on developing a multifunctional ligand with an ability to induce β-amyloid fibril (fAβ) disaggregation and to stimulate neurite outgrowth in fAβ-driven neurodegeneration. Such features do have the potential to be a promising therapeutic strategy for fAβ-driven AD patients. The authors synthesized a hydroxyalkylquinoline J2326; subsequently characterized its neurodegenerative potential in vitro and in vivo. The effects on aggregation kinetics, Aβ interaction analyses, and precise K determination involved SPR and BLI platforms. Equipped with super Streptavidin biosensors, the Pall ForteBio Octet system used in this investigation captured biotinylated Aβ1-42. The binding assays involved transferring of Aβ1-42 captured sensors into well containing varying concentrations of J2326.

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