Dr. Golde stresses a cautionary note. He worries that because of these findings, people with Alzheimer’s, or those who are at risk for developing the disease, might decide to take high doses of an over-the-counter AB42-lowering NSAID, such as ibuprofen. Because of the side effects associated with NSAID use, this could be quite harmful, he says. Indeed, because it does not inhibit COX at therapeutic levels, r-flurbiprofen is not an NSAID, whereas flurbiprofen is, he adds.
AB42-lowering agents may turn out to be “either a magic bullet or a magic shotgun,” he says. “They might be lowering AB42, reducing inflammation and doing five other things that we don’t know about.”
But to Mayo Clinic researchers, the big question is whether this compound, or any other similar kind of agent, can be used much earlier in people deemed to be at risk of developing Alzheimer’s.
“I think Alzheimer’s is going to be much easier to treat if you can prevent accumulation of AB in your brain, than if you try to treat it once plaques form,” Dr. Golde says. “We know that statins don’t work very well if a heart artery is 99 percent blocked, but do if they are taken earlier. The same thing would go for a drug designed to prevent Alzheimer’s.”
If r-flurbiprofen shows solid benefit in the phase III clinical trial, then it could be tested as a preventive agent, Dr. Golde says. But he adds that this “could possibly be the costliest trial ever to be conducted,” because it would take decades and involve thousands of people. However, Dr. Golde and his clinical colleagues share a common goal: to eventually conduct cost-effective prevention trials.
Restoring memory via tau
Mayo Clinic researchers also are working to prevent additional damage from occurring and to repair existing lesions in people who already have symptoms of Alzheimer’s.
In the process, they are attempting to answer the question that has stumped the