In Alzheimer’s disease, the problem is beta-amyloid, a protein that accumulates in the brain and causes nerve cells to weaken and die. Drugs designed to eliminate plaques made of beta-amyloid have a fatal problem: they need to enter the brain and remove the plaques without attacking healthy brain cells.
New research from the laboratory of Nobel Prize winner Paul Greengard, however, suggests that treatments modeled on the blockbuster cancer drug Gleevec could be the solution.
The findings are reported in the Sept. 2 issue of the journal Nature.
Gleevec, it turns out, has the unique ability to bind to a protein that triggers the production of beta-amyloid plaques. The new research from Greengard’s lab shows that this protein, called gamma-secretase activating protein (GSAP), dramatically and selectively increases the production of beta-amyloid peptide, which makes up the senile plaques found in the brains of most people with Alzheimer’s. GSAP works through a mechanism involving its interactions with gamma-secretase, an enzym