Alzheimer's Disease Vaccine Protects Mice
> 11/12/2007 2:56:02 PM

Last week, we covered the tantalizing progress of a smoking vaccine that reprograms the immune system to fight nicotine. Last month, a study in Neurology established a clear link between smoking and Alzheimer's Disease (AD) risk. In a fortunate coincidence, evidence has emerged suggesting that both smoking addiction and AD may be treatable with a similar technique. Scientists at the Oklahoma Medical Research Foundation (OMRF) recently reported initial success in using a vaccine to combat AD.

The OMRF researchers administered a vaccine for the enzyme memapsin 2 to mice that had been engineered to develop AD. Memapsin is suspected of causing AD by messily loosing the protein fragments that build plaques in the brain. The treated mice showed 35% less neural plaque, and they performed better on cognitive tasks.

The results of this animal trial are exciting, but must be examined with a critical eye. It is important to recognize that the trial rests upon two large assumptions: that these mice are valid analogs of humans, and that memapsin 2 causes AD. While mice have long been accepted as useful stand-ins for humans, it is very possible that their appreciably different bodies will respond to medical techniques in ways that vary from what we might expect in humans. This is particularly true for experiments that test the brain, the organ that most distinguishes humans from animals that share a large portion of their DNA. In addition to the problem of comparing mouse brains to human brains, there is the question of whether these engineered mice really have the same disease that wrecks humans. It is possible that they have been bred to exhibit similar symptoms without actually having the same underlying disease.

This question about the nature of the mouse AD leads to the second assumption on which the OMRF trial is based, that memapsin 2 causes AD. The disease is not fully understood, and the hypothesis about neural plaques is only one strong possibility among many. If neural plaque is just a symptom of another malfunction that causes dementia, then immunizing against it will not solve the basic problem. Just one example of an alternate hypothesis is the idea that AD is really a third form of diabetes.

In the OMRF press release, lead author Jordan Tang acknowledges that their success should be viewed with guarded optimism. Trying to stave off reports about a miracle cure, he stated:

Alzheimer's is a complicated, multi-faceted disease. As with illnesses like cancer and heart disease, Alzheimer's demands that we develop many different approaches to combat it.

Dr. Tang's caution likely stems from his knowledge of the 2001 announcement of an AD vaccine that helped mice but proved dangerous for humans. In that prior study, Dr. Thomas Wisniewski was so excited by a 89% plaque reduction that he assured:

We believe that our peptide vaccine isn't toxic to nerve cells because it doesn't aggregate into clumps; it remains in solution.

Despite his confidence, human trials were later shut down after 15 patients were imperiled by central nervous system swelling.

Dr. Tang's vaccine has been tailored to minimize the danger, and so it may be able to save millions of lives. Even if the more gentle vaccine only achieves 35% plaque reduction instead of 89%, it can still buy many sufferers a few more precious years of clarity. The AD vaccine has been difficult to achieve, but it is a goal worth working towards.

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