The leading hypothesis for Alzheimer’s Disease (AD) is the aggregation of amyloid beta plaques in the brain, but research has yet to definitively prove the role of the amyloid peptide in the pathology of the disease. Our work focuses on investigating the interaction of amyloid beta peptides with copper to study the effects on neurotoxicity and amyloid-beta aggregation in vivo. The interaction between amyloid beta and copper results in the production of reactive oxygen species. To combat this, we use copper chelating compounds to prevent the interaction between copper and amyloid beta. The effects of copper and the various copper chelate compounds on the mobility and lifespan of Caenorhabditis elegans (C. elegans) with Pan-neuronal amyloid beta1-42 expression have been studied in comparison to a control group. Copper chelation reduces the amount of reactive oxygen species produced in the brains of the C. elegans. There is also a positive relationship between a mixture of copper and the copper chelator, beta-alanine, and increased lifespan in the experimental C. elegans. This suggests that the increased lifespan on the C. elegans occurs because beta alanine binds to copper (and potentially other metals), reducing the overall formation of reactive oxygen species in neuronal.

Investigating the effects of copper and copper chelating compounds on Caenorhabditis elegans with pan-neuronal amyloid beta 1-42 expression

Fall 2022 abstracts, posters, and presentations will launch in mid-September.

ACS Fall 2022

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.