Inhibition of amyloid beta toxicity in zebrafish with a chaperone-gold nanoparticle dual strategy.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 31439844.
- Also identified by DOI 10.1038/s41467-019-11762-0 and PMC identifier 6706415.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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 Aβ<sub>42</sub> 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.
Medical subject headings
- Alzheimer Disease
- Amyloid beta-Peptides
- Chelating Agents
- Drug Carriers
- Metal Nanoparticles
- Peptide Fragments