As they report in the international open-access medical journal PLoS Medicine, they have engineered mice to continuously produce Abeta in their brains. The production can be switched off by giving the mice the antibiotic tetracycline in their drinking water. This switch-off at a certain point is similar to what would happen to human patients who would receive enzyme inhibitors once diagnosed with AD. Without tetracycline, the brains of the mice at six months of age are loaded with amyloid plaques. When the researchers switched the system off after some initial plaques had formed, they found two things: the existing plaques didn't grow or spread to other areas of the brain, but they did not go away either.
As always, results from animal models cannot simply be extrapolated to human disease. However, this study suggests that treatment with drugs that lower production of Abeta can prevent progression of AD but not reverse the disease. While overall encouraging, the results emphasize the importance of early treatment with drugs that inhibit Abeta production.
Citation: Jankowsky JL, Slunt HH, Gonzales V, Savonenko AV, Wen JC, et al. (2005) Persistent amyloidosis following suppression of Ab production in a transgenic model of Alzheimer disease. PLoS Med 2(12): e355.
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