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Science Advances|March 3, 2016
An anticancer drug suppresses the primary nucleation reaction that initiates the production of the toxic Aβ42 aggregates linked with Alzheimer's diseaseJohnny Habchi, Paolo Arosio, Michele Perni, et al.Nature Communications|August 17, 2024
α-Synuclein oligomers form by secondary nucleationCatherine K Xu, Georg Meisl, Ewa A Andrzejewska, et al.Chemical Science|May 17, 2024
Molecular mechanism of α-synuclein aggregation on lipid membranes revealedAlexander J Dear, Xiangyu Teng, Sarah R Ball, et al.Nature Structural & Molecular Biology|September 29, 2020
Kinetic fingerprints differentiate the mechanisms of action of anti-Aβ antibodiesSara Linse, Tom Scheidt, Katja Bernfur, et al.Molecular Cell|May 7, 2016
The S/T-Rich Motif in the DNAJB6 Chaperone Delays Polyglutamine Aggregation and the Onset of Disease in a Mouse ModelVaishali Kakkar, Cecilia Månsson, Eduardo P de Mattos, et al.Nature Communications|January 16, 2019
Trodusquemine enhances Aβ42 aggregation but suppresses its toxicity by displacing oligomers from cell membranesRyan Limbocker, Sean Chia, Francesco S Ruggeri, et al.Acta Neuropathologica|April 22, 2019
Galectin-3, a novel endogenous TREM2 ligand, detrimentally regulates inflammatory response in Alzheimer's diseaseAntonio Boza-Serrano, Rocío Ruiz, Raquel Sanchez-Varo, et al.Cell Stress & Chaperones|December 21, 2025
J-domain proteins: from molecular mechanisms to diseasesJanine Kirstein, Rina Rosenzweig, Paolo De Los Rios, et al.Pageof 35