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Fatty Acid in Fish May Arrest Alzheimer's

Mice deficient in DHA show significant memory loss

WEDNESDAY, Sept. 1, 2004 (HealthDayNews) -- A diet rich in the omega-3 fatty acid called DHA, which is found in salmon, halibut, and other cold-water fish, protects the brain from the damage caused by Alzheimer's disease, a new study says.

While the research, which appears in the Sept. 2 issue of Neuron, involved only animals, the premise is based on human studies focusing on risk factors for Alzheimer's disease, said study author Greg Cole, a professor of medicine and neurology at UCLA's David Geffen School of Medicine.

Many studies have shown an association between low DHA (docosahexaenoic acid) intake and increasing risk of Alzheimer's disease, Cole said. A constant supply of DHA is crucial for normal brain function in humans.

Cole's team focused on altering the diet of lab mice once they were 17 months old, after feeding them a normal diet high in omega-3 fatty acids during their infancy.

They studied mice bred with genetic mutations that cause the lesions linked to advanced Alzheimer's, assigning them to one of three groups. "Group one continued on the diet they had always gotten," Cole said. "Group two was put on a special diet with no DHA. Group three's diet had more DHA than the diet they grew up on."

Three other groups of mice without the genetic mutations, serving as controls, were given the same three diets as the genetically altered mice.

After five months, the researchers compared the mice on the different diets.

The mice with the genetic mutations fed a DHA-deficient diet had high amounts of damage to their synapses, the chemical connections between the brain's neurons that help the flow of information, Cole said. The changes resemble what is see in the brains of people with Alzheimer's, he added.

"The [DHA-deficient] diet and the Alzheimer's gene interact to cause a deficit of DHA in the brains of the animals," Cole said.

The mice on the DHA-deficient diet with the genetic mutation had 90 percent more synaptic loss compared to those with the genetic mutation fed the DHA-rich diet, Cole said.

On memory tests given the animals, those with the genetic mutation whose diets had no DHA took twice as long to perform on a test of spatial memory, said study co-author Sally Frautschy, an associate professor of medicine at UCLA and a research health scientist at the Greater Los Angeles Health Care System. The test would be roughly equivalent to a human trying to remember where he parked his car, she said.

The study breaks new ground because "it shows the disease itself depletes our brain of DHA through oxidation, and you can correct it by putting it back [via a DHA-rich diet]," Frautschy said. "The study shows that replenishing the DHA can arrest the development of Alzheimer's, at least in animals."

Added Cole: "We have evidence that DHA works as a risk factor for Alzheimer's disease from associated studies. We know DHA is getting oxidized in the brains of Alzheimer's patients. And it's practically harmless to add it back to your diet."

About 4.5 million Americans have Alzheimer's disease, according to the Alzheimer's Association. The complex and progressive disease destroys brain cells and robs sufferers of their memory.

"It's a good study, done in a good place," said Bill Thies, vice president for medical and scientific affairs for the Alzheimer's Association. "The only thing we have to remember is it's a study done in mice, and mice aren't people."

But Thies adds that the findings are "consistent with a growing body of evidence that makes risk factors for heart disease correlate with those for Alzheimer's disease." For instance, he said, "we already know that omega-3 fatty acids seem to have an impact on heart disease, and it's possible that eating more fish reduces heart disease."

Cole and Frautschy suggest that people consider taking DHA supplements in the form of fish oil capsules or eating more fish or omega-3 enriched eggs. But Thies prefers to advise people to simply eat more fish, echoing the advice of the author of the editorial accompanying the study.

More information

For more information on preventing the disease, visit the Alzheimer's Association.

SOURCES: Bill Thies, Ph.D., vice president, medical and scientific affairs, Alzheimer's Association, Chicago; Greg Cole, Ph.D., professor, medicine and neurology, UCLA David Geffen School of Medicine, Los Angeles; Sally Frautschy, Ph.D., associate professor, medicine, UCLA David Geffen School of Medicine, and research health scientist, Greater Los Angeles Health Care System, Los Angeles; Sept. 2, 2004, Neuron
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