Researchers Seek Vaccine to Prevent Alzheimer's

Three new studies in mice are giving weight to the idea that an Alzheimer's vaccine may work in humans. Such a vaccine is already in the early stages of a study in humans, and researchers say these latest findings in animals bolster the hope that a vaccine may prevent or treat the devastating brain disease.

All thee studies, published in the December 21/28 issue of Nature, demonstrate that particular physical changes seen in the brains of Alzheimer's patients are correlated with the memory loss and other symptoms of the disease. More important, two of the studies showed that preventing the physical damage with a vaccine may also prevent Alzheimer's symptoms.

The studies all involved mice genetically engineered to display some of the characteristics of the human Alzheimer's disease. In each study, investigators focused on substances call beta-amyloid proteins, which are constituents of the "plaques" that accumulate in the brains of Alzheimer's patients.

Experimental vaccines are targeting the beta-amyloid proteins, with the hope that preventing amyloid deposition may prevent or slow the development of some Alzheimer-associated symptoms.

Dr. David Westaway of the University of Toronto, Canada, was a co-author on one of the studies. He told Reuters Health that the first experiments with beta-amyloid vaccines focused on whether they could keep plaques from forming. These animal findings, he Said, show that vaccination may prevent the "real clinical presentation" of Alzheimer's — specifically, certain types of learning and memory problems.

The principle behind that Alzheimer's vaccine is similar to that of any vaccine. Researchers believe that exposing people to a small amount of beta-amyloid protein will train their immune systems to fight the build-up of plaques in the brain. Animal research has already suggested vaccination may clear plaques. Now, Westaway said, there is evidence that doing this prevents Alzheimer's-like symptoms.

"We don't know if this will happen in humans," he said. "But with mice, we now have a proof of principle."

Westaway's team and another research group led by Dr Dave Morgan of the University of South Florida in Tampa demonstrated that vaccinated mice retained their ability to wend through a water maze, while untreated mice showed declines. The treated mice also had a reduction in brain plaques.

In an editorial accompanying the reports, Paul F. Chapman of Cardiff University, UK, calls the studies "cause for optimism." "Their results support the previous observation of a reduction in the formation of amyloid deposits," he writes. "But they go further, to show that immunization also offers the mice some protection from the "spatial" learning deficits that normally accompany plaque formation."

However, whether the vaccination wards off other types of cognitive losses remains unknown, according to Chapman. And, he notes, some researchers believe another protein called tau is at least equally as important as beta-amyloid in Alzheimer's. If this is true, Chapman writes, a beta-amyloid vaccine may be ineffective.

But if it is effective in humans, according to West away, the first use will be in preventing Alzheimer's. "We want to catch it early on," he said. "But it may be possible to treat it in more advanced stages, too."

About 4 million Americans have Alzheimer's disease, and experts predict that over the next 50 years that number will jump to 14 million if no effective prevention is developed.



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