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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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