recent study published in the Journal of Neurochemistry, researchers observed the effects of TCT on neurological damage that can be caused in two different ways: through the presence of homocysteic acid, which in excess can cause vascular and neuronal lesions associated with cardiovascular disease, and the fatty acid linoleic acid, which can directly stimulate damaging free radical activity. Fatty acids are related to stroke: They rapidly accumulate when a clot in a vessel stops blood flow to the brain, and play a role in irreversible brain injury.

To observe the TCT's effectiveness, rodent neural cells were pretreated with extremely low concentrations of TCT; these cells avoided the cell death associated with toxicity caused by homocysteic acid. But to reduce free-radical activity and resulting neurotoxicity, the scientists found that a higher concentration of TCT was needed: Tocotrienol does not exhibit antioxidant properties until it reaches a concentration 10 to 25 times stronger than the concentration that prevented the cell death signal.

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Source:Ohio State University


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