Microchip Circulation Drastically Accelerates Amyloid Aggregation of 1-42 β-amyloid Peptide from Felis catus.

The amyloid aggregation process of amyloid β1-42 peptide is responsible for Alzheimer's disease, affecting millions of elderly people worldwide. Although there has been a great deal of attention directed toward tackling this disease, still no medicine has been found for this fatal disorder. To address this challenge, it is vital to thoroughly understand the molecular mechanism underlying the amyloid peptide aggregation process, as well as seek substances that could hamper this aggregation. In order to shed light on mechanisms leading to amyloidogenesis, we employed a microfluidic system to determine the possible influence of in vivo-like flow in the microchip channel itself on feline Aβ1-42 peptide amyloidogenesis. We have shown that shear forces occurring during such flow immensely accelerated peptide aggregation. We also tested the inhibitory influence of 3,3'-[1,6-(2,5-dioxahexane)]bis(1-dodecylimidazolium) dichloride gemini surfactant on peptide amyloidogenesis. Our results suggest that this surfactant may inhibit amyloid β1-42 fibril formation.