Light‐Controlled Toxicity of Engineered Amyloid β‐Peptides

Abstract

Aggregation of amyloid β (Aβ(1-42)), causing toxicity, is a critical step in Alzheimer's disease (AD). AD studies are difficult to compare because Aβ(1-42) aggregation is poorly controllable under physiological conditions. To control aggregation and toxicity, we engineered light-switchable Aβ(1-42) analogues that enable controllable conversion of nontoxic fibrils into toxic oligomers simply by illumination.