Conclusions

The modeling of AD, much like the modeling of many other human diseases, has been partially successful, but is in need of further refinement. Many, but not all, of the aspects of the AD phenotype have been reproduced in animal models. It is too early to know whether the models will be predictive of therapeutic efficacy in humans of the different agents currently being tested. That is a hurdle that all models for testing interventions must clear. The models have already proven extremely valuable for hypothesis testing and exploration of molecular mechanisms of disease.

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