The Omega-3 you may be taking to help prevent Heart Disease can also lower your risk of Alzheimer’s

UCLA neuroscientists have shown for the first time that a diet high in the omega-3 fatty acid DHA helps protect the brain against the memory loss and cell damage caused by Alzheimer's disease. The new research suggests that a DHA-rich diet may lower one's risk of Alzheimer's disease and help slow progression of the disorder in its later stages. The journal Neuron reported the findings on September 2, 2004.

"This is the first proof that our diets affect how our brain cells communicate with each other under the duress of Alzheimer's disease," said Greg Cole, senior author and a professor of neurology at the David Geffen School of Medicine at UCLA. "We saw that a diet rich in DHA, or docosahexaenoic acid, dramatically reduces the impact of the Alzheimer's gene".

"Consuming more DHA is something the average person can easily control," added Cole, associate director of the UCLA Alzheimer's Disease Research Center. "Anyone can buy DHA in its purified form, fish-oil capsules, high-fat fish or DHA-supplemented eggs."

Cole and his colleagues focused on Alzheimer's damage to synapses — the chemical connections between brain cells that enable memory and learning.

By using mice bred with genetic mutations that cause the brain lesions linked to advanced Alzheimer's disease, the UCLA researchers created a mouse model to test environmental risk factors for the disorder. When the mice developed the lesions, but showed minimal memory loss or synaptic brain damage, however, the scientists took a closer look at the animals' diet.

"We discovered that the mice lived on a nutritious diet of soy and fish — two ingredients chock-full of omega-3 fatty acids," said Sally Frautschy, co-author and an associate professor of neurology at the school.

"Because earlier studies suggest that omega-3 fatty acids may prevent Alzheimer's disease, we realized that the mice's diet could be countering the very thing we were trying to accomplish — showing the progression of the Alzheimer's-related brain damage," she said.

The UCLA team swapped safflower oil for the soy and fish to create an unhealthful diet depleted of omega-3 fatty acids. They divided the animals into two sets of older mice, which already showed brain lesions but displayed no major loss of brain-cell activity. The researchers placed both groups on the new diet, but fed the second group DHA supplements.

After five months, the researchers compared each set of mice to a control group that consumed the same diet but did not carry the Alzheimer's genes. The results surprised them. "We found high amounts of synaptic damage in the brains of the Alzheimer's-diseased mice that ate the DHA-depleted diet," Frautschy said. "These changes closely resembled those we see in the brains of people with Alzheimer's disease."

Although the mice on the DHA-supplemented diet also carried the Alzheimer's genes, they still performed much better in memory testing than the mice in the first group.

"After adjusting for all possible variables, DHA was the only factor remaining that protected the mice against the synaptic damage and memory loss that should have resulted from their Alzheimer's genes," Cole said. "We concluded that the DHA-enriched diet was holding their genetic disease at bay."

The human brain absorbs DHA rapidly, making a constant supply critical for proper cognitive function, eye development and mental tasks. DHA helps keep the brain membrane fluid, moves proteins and helps to convert signals from other parts of the body into action.

Cheap sources of DHA include coldwater fish, like salmon, halibut, mackerel, sardines and herring. These fish consume algae, which is high in DHA. Because these fishes' oiliness makes them absorb more mercury, dioxin, PCP and other metals, however, a less risky strategy is to consume fish oil or purified DHA supplements.

Cole and Frautschy also are researchers at the Greater Los Angeles Veterans Affairs Healthcare system. The National Institute on Aging, National Institute of Neurological Diseases and Stroke, and Canadian Institutes of Health Research funded the study. Co-authors included Frederic Calon, Giselle Lim, Fusheng Yang, Takashi Morihara, Bruce Teter and Oliver Ubeda of the VA and the David Geffen School of Medicine at UCLA. Other collaborators included Phillippe Rostaing, Antoine Triller, Norman Salem Jr. and Karen Ashe, who developed the mouse model.