According to the amyloid hypotheses Alzheimer’s disease is characterized by the accumulation and aggregation of the A-beta-peptide, which leads to hyperphosphorylation of Tau and neuronal cell death. However, the exact mechanisms leading to this phenomenon are still not well understood. To investigate this issue we used 11 different mouse models of AD, deficient for several ABC transporters, and a systems biology approach. Using this approach we were able to show the impact of these transport proteins on the clearance of A-beta from the brain. Moreover, we provide evidence that the induction of such transport proteins can result in reduced A-beta burden. Thus, the induction of ABC-transporters provides a new option for future AD treatment strategies.