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During the past years lots of research has been done on Alzheimer’s disease, but so far without any success in producing a preventative or even therapeutic treatment. Since we are facing an Alzheimer epidemic in the near future, a highly accessible and affordable preventative strategy is still eagerly awaited. Natural compounds have become of great importance and in particular green tea polyphenols have gained lots of attention. These polyphenols are believed to have neuroprotective effects due to different mechanisms like antioxidant and iron chelating abilities. The aim of our study was to investigate if we could objectify a preventative efficacy of green tea supplementation in a mouse model of AD. For this research we used 28 mice that were either wild type or transgenic mice of the APPPS1-21 strain, which is a well-established mouse model in the field of AD research. Mice were randomly assigned to a green tea supplementation or mock treatment shortly before amyloid deposition was supposed to occur in the hippocampal dentate gyrus of transgenic mice. At this moment the transgenic mice are still in a pre-symptomatic stage without observable behavioral symptoms. After 21 weeks of green tea administration, mice reached the age where they should start showing behavioral signs of underlying cognitive deficits. From then on, all mice were subjected to a battery of behavioral tests to examine whether or not significant effects of treatment were found. During the behavioral tests, the treatment was continued. We hypothesized that transgenic mice receiving green tea supplemented water would show improvement of cognitive and/or other impairments. Unfortunately no such clear effects were found. On some tests there was an effect of genotype, confirming that the mice showed cognitive deficits. For example they showed a slower learning curve on the MWM than wild type mice. Effects regarding the green tea administration were rather rare, but we cannot be certain that the green tea supplementation had no effect due to the good performance of transgenic mice receiving mock treatment on some tests. Based on the tests where transgenic mice did show a clear deficit but no treatment effects were found, we have to conclude that we failed to objectify a preventative efficacy of green tea supplementation in a mouse model of AD, but further research on this topic is recommended.