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Transthyretin Inhibits Primary and Secondary Nucleations of Amyloid-β Peptide Aggregation and Reduces the Toxicity of Its Oligomers

Seyyed Abolghasem Ghadami, Sean Chia, Francesco Simone Ruggeri, Georg Meisl, Francesco Bemporad, Johnny Habchi, Roberta Cascella, Christopher M. Dobson, Michele Vendruscolo, Tuomas P. J. Knowles, Fabrizio Chiti

2020Biomacromolecules79 citationsDOIOpen Access PDF

Abstract

, while maintaining its overall topology. Hence, it is likely that the predominant mechanism by which TTR exerts its protective role lies in the binding of TTR to the Aβ oligomers and in inhibiting primary and secondary nucleation processes, which limits both the toxicity of Aβ oligomers and the ability of the fibrils to proliferate.

Topics & Concepts

TransthyretinFibrilThioflavinChemistryAmyloid (mycology)PeptideBiophysicsSenile plaquesAmyloid diseaseOligomerProtein foldingIn vitroBiochemistryAmyloid fibrilAlzheimer's diseaseBiologyAmyloid βDiseaseOrganic chemistryPathologyMedicineInorganic chemistryEndocrinologyAlzheimer's disease research and treatmentsAmyloidosis: Diagnosis, Treatment, OutcomesCellular transport and secretion
Transthyretin Inhibits Primary and Secondary Nucleations of Amyloid-β Peptide Aggregation and Reduces the Toxicity of Its Oligomers | Litcius