Bin1 and CD2AP polarize Aβ generation in neurons

Mutations in the APP and PSEN genes have provided direct evidence for the central role of aberrant amyloid β (Aβ) peptide production in familial Alzheimer's disease (AD). Newly identified risk factors will further help us to unravel how derailed physiological and cell biological processes lead to identical pathogenesis in late‐onset AD (LOAD). Ubelmann et al now unveil in this issue how two of such risk factors, Bin1 and CD2AP, regulate the encounter of APP and BACE1 in axonal and dendritic endosomes, emphasizing endosomal transport balance as a critical factor in AD pathogenesis 1.