Vitamin E May Boost Brain Health After Stroke


May prevent nerve cell death in the brain following a stroke, suggests new research on this emerging form of Vitamin E.

Alpha-tocotrienol, one of eight forms of Vitamin E, was found to inhibit an enzyme from releasing fatty acids that eventually kill neurons, according to findings from a study with mouse brain cells published in the Journal of Neurochemistry.

The beneficial effects are observed at low levels of the nutrient, researchers from Ohio State University report following their National Institutes of Health-funded study.

"Tocotrienol - a natural dietary form of the nutrient Vitamin E, can be just as effective as drugs or other therapeutic agents, if not more so, in neural protection, opening up new possibilities into prevention and even treatment of stroke and other neuro-degenerative diseases" the researchers noted.

The potential neuroprotective effects of nanomolar levels of tocotrienol were first reported a decade ago. This latest study from The Ohio State University helps clarify how Vitamin E tocotrienol, which is easily achievable by daily supplementation, protects the brain in artificially induced stroke," they added.

"It shows tocotrienol inhibits the enzyme cPLA2 from releasing arachidonic acid into the brain. The release of arachidonic acid is an important step in causing neuronal death from glutamate induced state which mimics stroke," explained the researchers.

There are eight forms of vitamin E: four tocopherols (alpha, beta, gamma, delta) and four tocotrienols (alpha, beta, gamma, delta). Alpha-tocopherol is the main source found in supplements and in a healthy European diet, while gamma-tocopherol is the most common form found in the American diet. Tocotrienols are only minor components in plants, although several sources with known high levels include palm oil, cereal grains and rice bran.

The scientists involved in the study looked at the effects of alpha-tocotrienol to inhibit the action of the enzyme called cystolic calcium-dependent phospholipase A2, or cPLA2. Following the trauma of blocked blood flow associated with a stroke, an excessive amount of the neurotransmitter glutamate is released in the brain. Despite having an important role in learning and memory, too much glutamate can trigger the death of brain cells, or neurons, said to be the most damaging effects of a stroke.

When tocotrienol was introduced to cells exposed to the high levels of glutamate arachidonic acid levels decreased by 60 per cent, said the researchers. This resulted in a cell survival rate four times higher than cells exposed to glutamate alone.

They noted that the effects were observable with a dose of tocotrienol, equivalent to a concentration about 10 times lower than the average amount of tocotrienol circulating in humans who consume the vitamin regularly.

Source: Journal of Neurochemistry Published online


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