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Inhibition of amyloid beta toxicity in zebrafish with a chaperone-gold nanoparticle dual strategy

Author

Listed:
  • Ibrahim Javed

    (Monash University
    Tongji University)

  • Guotao Peng

    (Tongji University)

  • Yanting Xing

    (Clemson University)

  • Tianyu Yu

    (Tongji University)

  • Mei Zhao

    (Tongji University)

  • Aleksandr Kakinen

    (Monash University)

  • Ava Faridi

    (Monash University)

  • Clare L. Parish

    (The University of Melbourne)

  • Feng Ding

    (Clemson University)

  • Thomas P. Davis

    (Monash University
    The University of Queensland)

  • Pu Chun Ke

    (Monash University)

  • Sijie Lin

    (Tongji University)

Abstract

Alzheimer’s disease (AD) is the most prevalent form of neurodegenerative disorders, yet no major breakthroughs have been made in AD human trials and the disease remains a paramount challenge and a stigma in medicine. Here we eliminate the toxicity of amyloid beta (Aβ) in a facile, high-throughput zebrafish (Danio rerio) model using casein coated-gold nanoparticles (βCas AuNPs). βCas AuNPs in systemic circulation translocate across the blood brain barrier of zebrafish larvae and sequester intracerebral Aβ42 and its elicited toxicity in a nonspecific, chaperone-like manner. This is evidenced by behavioral pathology, reactive oxygen species and neuronal dysfunction biomarkers assays, complemented by brain histology and inductively coupled plasma-mass spectroscopy. We further demonstrate the capacity of βCas AuNPs in recovering the mobility and cognitive function of adult zebrafish exposed to Aβ. This potent, safe-to-use, and easy-to-apply nanomedicine may find broad use for eradicating toxic amyloid proteins implicated in a range of human diseases.

Suggested Citation

  • Ibrahim Javed & Guotao Peng & Yanting Xing & Tianyu Yu & Mei Zhao & Aleksandr Kakinen & Ava Faridi & Clare L. Parish & Feng Ding & Thomas P. Davis & Pu Chun Ke & Sijie Lin, 2019. "Inhibition of amyloid beta toxicity in zebrafish with a chaperone-gold nanoparticle dual strategy," Nature Communications, Nature, vol. 10(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:10:y:2019:i:1:d:10.1038_s41467-019-11762-0
    DOI: 10.1038/s41467-019-11762-0
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    Cited by:

    1. Yuhuan Li & Nengyi Ni & Myeongsang Lee & Wei Wei & Nicholas Andrikopoulos & Aleksandr Kakinen & Thomas P. Davis & Yang Song & Feng Ding & David Tai Leong & Pu Chun Ke, 2024. "Endothelial leakiness elicited by amyloid protein aggregation," Nature Communications, Nature, vol. 15(1), pages 1-18, December.

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