Bridging the gap between cellular amyloid metabolism and Alzheimer’s disease clinical data

Alzheimer’s disease (AD) diagnosis strongly correlates with the density of amyloid deposits. Yet, amyloid fibrils per se are not toxic, which represents a major gap in amyloid‐based theories of AD. Based on the proposed previously amyloid degradation toxicity hypothesis, we present the mathematical model of amyloid turnover that bridges this gap (Fig.1).