We found that AD mutations in APP and PSEN1 markedly disrupted the axonal transport of lysosomes and those lysosomes accumulate within distal axons contained low levels of cathepsin D. This is similar to previous findings in human AD brain tissue as well as various AD mouse models in which focal axonal swellings containing accumulations of lysosomal dense bodies and autophagic vacuoles have been observed (Nixon, 2017). Here, CTSD is linked to Alzheimer disease.