In the amyloid cascade, misprocessing of the amyloid precursor protein (APP) in the brain leads to the formation of Aβ peptides (Aβ40 and Aβ42) which undergo self‐assembly to form neurotoxic species such as oligomers, protofibrils and fibrils which promote neurodegeneration, and also trigger other secondary events to cause brain damage in AD.[4, 8] Understanding the molecular mechanisms of Aβ self‐assembly into toxic β‐sheet structures is a daunting task. Here, APP is linked to Alzheimer disease.