Abstract: Objective To study the axon abnormalities and possible underlying mechanisms on APPswe/PS1dE9 double-transgenic mice, as the model of Alzheimer’s disease (AD). Methods Taking advantage of RT-qPCR, the expression levels of netrin (netrin-1 and netrin-3) and DCC (DCC1 and DCC2) are determined in wild type mice and APPswe/PS1dE9 double-transgenic mice separately, while the changes of axon length in hippocampus neurons are calculated using immunocytofluorescence. Results Compared with wild type mice, the expression levels of netrin-1 (P<0.001), DCC1 and DCC2 (P<0.01) are all up regulated in APPswe/PS1dE9 double-transgenic mice. At the same time, the double transgenic mice show decrease in axon length in hippocampus neurons. Conclusions Abnormalities in axon are found in connection with AD, and interactions in netrin-1 and DCC can be responsible for this relationship.

Key words: Alzheimer’s Disease, APPswe/PS1dE9, axon, netrin, DCC