LOS ANGELES, CA (Catholic Online) - The mutation appears to slow the production of the beta-amyloid protein which has long been considered a cause of Alzheimer's. One of the prevalent theories about Alzheimer's is that beta-amyloid plaques cause this form of dementia.. Dr. Kari Stefansson, chief executive of the Icelandic company DeCode Genetics studied data from the genomes of nearly 1,800 Icelandic people.

The catch?  At first glance, the genetic test for the protective mutation seems to be illogical. In order to determine if an individual has the gene - doctors wouldn't be able to detect it. Dr. Sam Gandy, director of the Mount Sinai Center for Cognitive Health, says this approach would require a specialized research lab.

Mutations like this are "not so good for screening as they are for teaching what's going on," said Rudolph Tanzi. Tanzi is a Harvard Medical School neurologist who was not involved in the study.

Attempts to clear some of the plaque out have failed to reverse the effects of dementia in clinical trials. However, Tanzi said that the new study drives home that targeting beta-amyloid is still the correct appraoch,

It appears that the drugs which have failed thus far weren't getting into the brain. Tanzi said that others had harmful side effects or were just defective. A new wave of clinical trial results will come this fall. If they fall short of their goals, this study will only lead to researchers to continue pursue the beta-amyloid.

"These are just not yet the right drugs and I think the right ones are yet to come," Tanzi says.

Dr. Robert Green, associate director of medicine in the division of genetics at Brigham and Women's Hospital and Harvard Medical School offers believes this would take years.

Finding a successful protective drug against Alzheimer's will probably have to be taken for decades, like a statin to reduce risk of heart problems, Green says. It could then become something everyone takes and perhaps the people most at risk of Alzheimer's would simply start on it earlier.

The study suggests that when someone has this specific mutation, the amount of beta-amyloid protein released into his or her brain - which contributes to Alzheimer's - might be reduced by as much as 40 percen. This might explain the lower rates of dementia.

For most of us, who do not have this mutation, beta-amyloid protein gets released when the amyloid precursor protein (APP) in a brain cell is cut by two enzymes: Beta-secretase and gamma-secretase.

Drug developers have tried inhibiting gamma-secretase, but because that enzyme is responsible for so many other important things, these drugs proved to be toxic. "You can't just hit it with a sledgehammer," Tanzi explains.

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