Visualizing APP and BACE-1 approximation in neurons yields insight into the amyloidogenic pathway

myloid-β (Aβ) is generated by BACE-1-mediated cleavage of amyloid precursor protein (APP), and its deposition is a pathological hallmark of Alzheimer's disease. The authors find that APP and BACE-1 interact in biosynthetic and endocytic compartments in neurons. In axons, APP and BACE-1 interact during cotransport. The Alzheimer's disease–protective Icelandic mutation attenuates these interactions, suggesting a mechanism of protection.