Endocytosis is implicated in Alzheimer’s pathogenesis, because the continuous swallowing up of proteins from the cell surface and packaging them into little organelles brings the amyloid precursor protein (APP) into contact with the secretases that chop it and produce Aβ. How this changes as cells age, though, and how genetic risk factors for Alzheimer’s influence it, is still unclear. Data presented at the14th International Conference on Alzheimer’s and Parkinson’s Diseases, held March 27–31 in Lisbon, Portugal, suggest that as cells get older, the endocytosis of APP speeds up, giving it more access to its cleaving enzymes and increasing its processing. Other presentations showed that over- or underexpressing certain endosomal factors brings on symptoms of disease, suggesting that too much or too little endocytosis could kick off intracellular disease before pathology accumulates.