Alzheimer's Drug May Actually Reverse The Progress Of The Disease

Illustration for article titled Alzheimer's Drug May Actually Reverse The Progress Of The Disease

A new method for detecting the levels of amyloid proteins in the brain, a key feature of Alzheimer's Disease, lets researchers figure out if a drug is reducing their prevalence, as one new drug has done. But there's a catch.


Alzheimer's is one of the most terrifying diseases out there, since it leaves people physically healthy but mentally ravaged. Researchers have long believed that amyloid plaques either cause Alzheimer's or are a key factor, and a lot of money has gone into researching drugs that reduce the prevalence of these plaques. So it's a great cause for celebration that bapineuzumab, a drug now being developed by Elan Corp. and now owned by Johnson & Johnson, showed an ability to reduce amyloid plaques in 28 patients.

At the end of the 18-month study period, the patients had 25 percent less amyloid plaques than a control group. And the bapineuzumab patients actually had less plaques than they had at the start of testing.

But actually, there are two catches here. The first is that bapineuzumab can have dangerous side effects — high doses can have ill effects, as earlier tests found, and two patients in the current study had cerebral edemas caused by water on the brain. But it sounds like the side-effects are manageable, and it may be just a matter of finding the right dosage.

The bigger catch is, we still don't know if amyloid plaques are a cause or merely a symptom of Alzheimer's disease. A large and growing number of researchers believe the true cause of Alzheimer's is the tangles of tau proteins that also accumulate in the brains of Alzheimer's sufferers. So it's possible that the decade of research into drugs that can reduce amyloid plaques will turn out to have been a blind alley. (Or it's possible that you need to attack both amyloid plaques and tau tangles, jointly.) It's notable that this latest study didn't actually track the mental functioning of the patients whose plaques were reduced.

In any case, whether bapineuzumab turns out to be a wonder drug, or a dead end, the real breakthrough here is the development of a method of assessing a patient's number of amyloid plaques — something we could only do after death, via autopsy, until now. Researchers were able to use a radiotracer called Pittsburgh compound B, which latches on to amyloid plaques in the brain, and then track it using PET scans. That could also be a valuable diagnostic tool, although it's not terribly useful until we actually have a treatment that works. [ and PhysOrg]



My dad, who died in January, had Alzheimers. Horrible horrible disease. Let's hope this drug, or another one, can soon fix the problem.