Alzheimer's Vaccine Shows Limitations
> 4/8/2008 8:19:48 AM

The cause of Alzheimer's Disease (AD) is not fully understood. When autopsies revealed that amyloid-beta plaque in the brain was a common denominator between patients with AD, doctors were quick to home in on the plaque in the search for better diagnostic and treatment methods. There are already multiple promising methods for detecting amyloid-beta levels before death. When researchers at the University of California, Irvine succeeded in developing a technique for destroying neural plaques, many were ready to pop the champagne. However, the latest clinical trial of the vaccine, presented in the April issue of the Journal of Neuroscience, shows that celebration is premature.

Dr. Elizabeth Head and her team studied a group of elderly dogs with symptoms of AD. At the beginning of the trial, half of these dogs were injected with a vaccine that trains their immune systems to recognize and attack amyloid-beta. At the end of two years, vaccinated dogs were able to consistently demolish amyloid-beta plaques, especially in the critical prefrontal cortex.

Despite the attainment of this target, the vaccine made little progress towards the ultimate goal of restoring mental abilities. Spatial attention and memory showed no improvement. The vaccinated dogs also scored the same on every learning task, except for a small recovery in reversal learning, an ability necessary for relearning a task to do the opposite of what was previously required. This small improvement was not enough to teach old dogs new tricks.

This assessment of cognitive benefit is very disappointing, but we are fortunate that researchers caught the disconnect between amyloid-beta and brain-function so early. Many patients are still reeling from the March discovery that Vytorin confers absolutely no heart benefits even though it reduces LDL. Both the researchers and the FDA were so sure of the connection between bad cholesterol and arterial plaque that approval was granted to the drug just for showing that it reduced the first part of the accepted chain. Now AD researchers can avoid the mistake of focusing only on neural plaque, treating it rather as one of multiple contributing factors.

Dr. Head admits that "reducing total amyloid-beta may be of limited therapeutic benefit" by itself, but her article suggests that it may help when combined with other methods. Canine autopsies revealed that even though the plaque was removed by vaccines, many of the newly freed neurons remained inactive. If plaque removal is followed by some sort of regenerative therapy, patients may very well have a chance of returning from the mist of dementia. If such regeneration proves impossible, the vaccine may work as a preventative measure administered to everyone when they reach a high-risk age.

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