NBD-BPEA regulates Zn- or Cu-induced Aβ aggregation and cytotoxicity.

Food Chem Toxicol

Institute of Nautical Medicine, Nantong University, Nantong, 226019, PR China. Electronic address:

Published: September 2018

Abnormal interaction of amyloid-β peptide (Aβ) and metal ions is proved to be related to the etiology of Alzheimer's disease (AD). Using metal chelators to reverse metal-triggered Aβ aggregation has become one of the potential therapies for AD. In our work, the effect of metal chelator, NBD-BPEA, on Zn- or Cu-mediated Aβ aggregation and neurotoxicity has been systematically studied. NBD-BPEA exhibits the capability to inhibit the metal-mediated Aβ aggregation and disassemble performed Aβ aggregates. It also prevents the formation of the β-sheet structure and promotes the reversion of the β-sheet to the normal random coil conformation. Moreover, it can alleviate Zn- or Cu-Aβ-induced neurotoxicity, suppress the intracellular ROS and protect against cell apoptosis. These preliminary findings indicate that NBD-BPEA has promising perspective of application in the treatment of AD, and therefore deserve further investigation as potential anti-AD agents.

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http://dx.doi.org/10.1016/j.fct.2018.03.035DOI Listing

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