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Negatively Charged Gold Nanoparticles Inhibit Alzheimer's Amyloid‐β Fibrillization, Induce Fibril Dissociation, and Mitigate Neurotoxicity
Author(s) -
Liao YiHung,
Chang YuJen,
Yoshiike Yuji,
Chang YunChorng,
Chen YunRu
Publication year - 2012
Publication title -
small
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.785
H-Index - 236
eISSN - 1613-6829
pISSN - 1613-6810
DOI - 10.1002/smll.201201068
Subject(s) - fibril , colloidal gold , neurotoxicity , chemistry , biophysics , amyloid fibril , amyloid (mycology) , nanoparticle , amyloid β , nanotechnology , biochemistry , toxicity , materials science , biology , organic chemistry , disease , medicine , inorganic chemistry , pathology
Amyloids are pathogenic hallmarks in many neurodegenerative diseases such as amyloid‐ β (A β ) fibrils in Alzheimer's disease (AD). Here, the effect of gold nanoparticles (AuNPs) on amyloids is examined using A β as a model system. It is found that bare AuNPs inhibited A β fibrillization to form fragmented fibrils and spherical oligomers. Adding bare AuNPs to preformed A β fibrils results in ragged species where AuNPs bind preferentially to fibrils. Similar results are demonstrated with carboxyl‐ but not amine‐conjugated AuNPs. Co‐incubation of negatively charged AuNPs with A β relieved A β toxicity to neuroblastoma. Overall, it is demonstrated that AuNPs possessing negative surface potential serve as nano‐chaperones to inhibit and redirect A β fibrillization, which could contribute to applications for AD.