Neurotrophins are one of the best-known examples of target-derived instructive cues that regulate distinct aspects of neuronal development. Upon nerve growth factor (NGF) binds to its receptor TrkA at axon terminals, these complexes are internalized and then retrogradely transported back to cell bodies. We have previously found the new function of retrograde signaling by which target-derived NGF enhances soma-to-axon transcytosis of TrkA. However, it is unclear whether the transcytosis machinery is a general mechanism which NGF utilizes to recruit additional membrane proteins necessary for axon growth and synapse maturation. Here we show evidence that NGF enhances soma-to-axon transcytosis of amyloid-beta precursor protein (APP). APP interacts with TrkA at the extracellular domain just adjacent to the transmembrane domain. Ectopic expression of APP induces the formation of neurite-like processes in non-neuronal cells, suggesting that transcytosis of APP with TrkA contributes to axon growth in neurons. Since APP and its proteolytic products play an important role in pathogenesis of Alzheimer's disease (AD), our data suggests that the TrkA-APP anterograde transcytosis is involved in NGF functioning and its defects might be related to the onset of AD.