Because new drugs designed to lower Aβ levels are still in development, they are not available for testing in animal models of the disease. Instead, basic questions about the effectiveness of this type of treatment must be answered using systems that mimic how the drugs work. To do this, the authors created mice that produce too much APP and that develop the same amyloid lesions as do human patients with AD. Unlike normal mice, these mice also carried a “switch” gene that allowed the researchers to turn off APP by feeding the mice special food. Turning off APP in these mice had the same effect as treating them with Aβ-lowering drugs, and so the researchers were able to ask what happened to the amyloid plaques after Aβ production was shut down. They showed that lowering Aβ production prevents the amyloid lesions from getting worse as the disease progresses. This means that treatment with Aβ-lowering drugs may be able to stop the disease from filling the brain with plaques. However, the researchers also found that the amyloid lesions that had formed before treatment was started remained intact throughout the experiment.