Martek's DHA algal oil reduces brain lesions in Alzheimer's animal model

Martek's proprietary DHA algal oil may slow the development of two brain lesions that are hallmarks of Alzheimer's disease, according to a study featured in the April 18 issue of the Journal of Neuroscience.

This pre-clinical study conducted at the University of California Irvine, with Martek support, used genetically modified mice. It is the first study to show that docosahexaenoic acid (DHA), an omega-3 fatty acid, may slow the accumulation of a protein, tau, that leads to the development of neurofibrillary tangles, one of two signature brain lesions of Alzheimer's disease. Confirming previous research, DHA also was found to reduce levels of another protein, beta amyloid, which can clump in the brain and form plaques, the other Alzheimer's lesion. Previous work has shown that DHA may have therapeutic value for Alzheimer's patients. This pre- clinical research is among the first to show that DHA may play a role in delaying the onset of the disease.

"We are greatly excited by these results, which show us that simple changes in diet can positively alter the way the brain works and lead to protection from Alzheimer's disease pathology," said Frank LaFerla, Professor of Neurobiology and Behavior and co-author of the study.

"The results of the research conducted by Dr. LaFerla and associates provide a potential mechanism of action for the beneficial role that DHA may have in delaying onset of the disease," said Steve Dubin, CEO of Martek. "We look forward to the results of additional research that will further evaluate the importance of DHA for cognitive function."

LaFerla and his research team studied the effects of Martek's microalgal DHA in mice bred to develop brain plaques and tangles associated with Alzheimer's disease. Mice in the control group were given chow that mimics a typical American diet, with the ratio of omega-6 fatty acids to omega-3 fatty acids being 10:1. Mice in three test groups were given chow with a balanced 1:1 ratio of omega-6 fatty acids to omega-3 fatty acids. One of these groups received supplemental DHA only with no long chain omega-6 fatty acids, and two groups received DHA with long chain omega-6 fatty acids. After three months, mice in all of the test groups had lower levels of beta amyloid and tau than mice in the control group; however, by nine months of treatment, mice on the DHA only diet had lower levels of both proteins while this effect was not seen in the other two test groups.

The scientists also determined the mechanism by which DHA leads to lower levels of beta amyloid. They found that DHA supplementation leads to lower levels of presenilin, an enzyme responsible for cutting beta amyloid from its parent, the amyloid precursor protein. Without presenilin, beta amyloid cannot be generated. When clumped into plaques, beta amyloid disrupts communication between cells and leads to symptoms of Alzheimer's disease.

Additional research investigating the effects of Martek's DHA on cognitive function is currently underway. A trial, co-sponsored by the National Institute of Aging (NIA) and being conducted by the Alzheimer's disease Cooperative Study (ADCS), is examining the effects of Martek's DHA in slowing the progression of cognitive and functional decline in patients with mild to moderate Alzheimer's disease. A second trial, sponsored by Martek, is evaluating the effects of Martek's DHA on age-related cognitive decline in healthy, older adults with mild memory complaints. For more information on these studies, visit www.clinicaltrials.gov.

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