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Negatively Charged Gold Nanoparticles Inhibit Alzheimer's Amyloid-β Fibrillization, Induce Fibril Dissociation, and Mitigate Neurotoxicity

Authors

  • Yi-Hung Liao,

    1. Institute of Biochemical Sciences, National Taiwan University, Taipei, Taiwan
    2. Genomics Research Center, Academia Sinica, Taipei, Taiwan
    3. Taiwan International Graduate Program, Chemical Biology and Molecular Biophysics Program, Academia Sinica, Taipei, Taiwan
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  • Yu-Jen Chang,

    1. Genomics Research Center, Academia Sinica, Taipei, Taiwan
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  • Yuji Yoshiike,

    1. Alzheimer's Disease Project Team, National Center for Geriatrics and Gerontology, Aichi, Japan
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  • Yun-Chorng Chang,

    Corresponding author
    1. Department of Photonics and Advanced Optoelectronic Technology Center, National Cheng Kung University, Tainan 701, Taiwan
    • Department of Photonics and Advanced Optoelectronic Technology Center, National Cheng Kung University, Tainan 701, Taiwan
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  • Yun-Ru Chen

    Corresponding author
    1. Institute of Biochemical Sciences, National Taiwan University, Taipei, Taiwan
    2. Genomics Research Center, Academia Sinica, Taipei, Taiwan
    3. Taiwan International Graduate Program, Chemical Biology and Molecular Biophysics Program, Academia Sinica, Taipei, Taiwan
    • Institute of Biochemical Sciences, National Taiwan University, Taipei, Taiwan.
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Abstract

Amyloids are pathogenic hallmarks in many neurodegenerative diseases such as amyloid-β (Aβ) fibrils in Alzheimer's disease (AD). Here, the effect of gold nanoparticles (AuNPs) on amyloids is examined using Aβ as a model system. It is found that bare AuNPs inhibited Aβ fibrillization to form fragmented fibrils and spherical oligomers. Adding bare AuNPs to preformed Aβ 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 Aβ relieved Aβ toxicity to neuroblastoma. Overall, it is demonstrated that AuNPs possessing negative surface potential serve as nano-chaperones to inhibit and redirect Aβ fibrillization, which could contribute to applications for AD.

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