The drug Gleevec was approved for treatment of chronic myelogenous leukemia (CML) in May of 2001. Paul Greengard of Rockefeller University and his colleagues investigated whether the drug can curtail the production of beta-amyloid, which forms the basis of the toxic plaques that interfere with brain function in people suffering from Alzheimer's. The researchers tested Gleevec in immature rat neurons and cultured human cells and found that levels of beta-amyloid decreased compared to control cells. What is more, the drug had a similar effect in live guinea pigs that have amyloid peptides comparable to those found in humans, with declines of up to 50 percent relative to control animals reported.
The results "may prove useful as a basis for developing novel therapies for Alzheimer's disease," the authors note. They caution, however, that the work is still very preliminary. For one, it is unclear whether Gleevec's ability to penetrate the blood-brain barrier will be sufficient to achieve therapeutic benefits.