Research

Electrochemical field key to how dementia precursors ‘break bad’

Amyloid beta peptides start out as helpful scaffolding, but they can turn toxic with the production of reactive oxygen molecules. Researchers at Washington University in St. Louis have found a new way to interrupt the toxic spread of these peptides. (Image: Michael W. Chen and Wenjing Li)
View Content

Protein accumulations do important work in the human body, but something can go wrong and proliferate in those aggregates, resulting in neurodegeneration and diseases such as Parkinson’s and Alzheimer’s.

One such assembly, amyloid beta peptide, is synonymous with dementia, but researchers were not certain how these peptide assemblies “break bad” and what really causes them to assemble.