New research has found that a component of fish oil reduced brain damage in mice following a stroke, according to a press release from Columbia University Medical Center. That’s what happened in layman’s terms.
Here is what happened in Columbia’s language: Triglyceride lipid emulsions rich in an omega-3 fatty acid injected within a few hours of an ischemic stroke decreased the amount of damaged brain tissue by 50 percent or more in mice. An ischemic stroke occurs when an artery to the brain is blocked.
The hope is that this research may be uncovering a treatment for humans with strokes.
According to the Columbia researchers, the research results suggest that the emulsions may be able to reduce some of the long-term neurological and behavioral problems seen in human survivors of neonatal stroke and possibly of adult stroke, as well. The findings were published last week in the journal PLoS One.
By way of background, Columbia said that clot-busting tPA (recombinant tissue-type plasminogen activator) is now the only treatment shown to improve recovery from ischemic stroke. The drug can restore blood flow to the brain but may not prevent injured, but potentially salvageable, neurons from dying, the press release said.
After 30 years of research, with more than 1000 agents tested in animals, no neuroprotectant drug has been found that can prevent the death of brain cells damaged by stroke in people, according to Columbia.
Omega-3 fatty acids may have more potential because they affect multiple biochemical processes in the brain that are disturbed by stroke, the study’s senior author, Dr. Richard Deckelbaum, director of the Institute of Human Nutrition at Columbia’s College of Physicians & Surgeons, said in a statement.
“The findings also may be applicable to other causes of ischemic brain injury in newborns and adults,” said co-investigator Dr. Vadim Ten, an associate professor of pediatrics from the Department of Pediatrics at Columbia.
Omega-3 fatty acids increase the production of natural neuroprotectants in the brain, reduce inflammation and cell death, and activate genes that may protect brain cells. Omega-3 fatty acids also markedly reduce the release of harmful oxidants into the brain after stroke, the press release said.
“In most clinical trials in the past, the compounds tested affected only one pathway,” Deckelbaum said. “Omega-3 fatty acids, in contrast, are very bioactive molecules that target multiple mechanisms involved in brain death after stroke.”
The study found that an emulsion containing only DHA (docosahexaenoic acid), but not EPA (eicosapentaenoic acid), in a triglyceride molecule reduced the area of dead brain tissue by about 50 percent or more even when administered up to two hours after the stroke, the press release said.
“Since mice have a much faster metabolism than humans, longer windows of time for therapeutic effect after stroke are likely in humans,” Deckelbaum said.
Eight weeks after the stroke, much of the “saved” mouse brain tissue was still healthy, and no toxic effects were detected.
Tests of the emulsion are now being conducted on older mice and in mice with different types of stroke, the press release said. Researchers are also conducting studies to figure out exactly how the omega-3 emulsion works and to optimize it in order to improve functional recovery after stroke.
After animal studies on dosages and timing, and if the emulsions continue to show promising results, Deckelbaum said, clinical trials could begin quickly, as such emulsions have already been shown to be safe in people.
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