A series of experiments reported in the October 1 2005 issue of the American Heart Association journal Stroke found that the form of vitamin E known as alpha-tocotrienol helped protect against brain damage in an animal model of stroke. Vitamin E consists of alpha, beta, gamma and delta tocopherol as well as four tocotrienols which can be deficient among many individuals.
Based on their previous finding that alpha-tocotrienol blocked neuronal death induced by glutamate (which is released by injured cells following a stroke) researchers at Ohio State University administered glutamate to groups of neurons in which the cytoplasm of one cell had been injected with a nanomolar concentration of alpha-tocotrienol. Twenty-four hours after glutamate treatment, all cells except the one injected with tocotrienol had died in 90 percent of the cases among the experiments conducted.
The team discovered that the vitamin inhibits glutamate-induced 12-lipooxygenase (12-Lox) activation. In an in vivo experiment conducted by the researcher, mice bred to be deficient in 12-Lox in whom stroke was induced were found to possess a greater resistance to brain injury than normal mice.
In another experiment, 32 spontaneously hypertensive rats were placed on vitamin E deficient diets until the induction of experimental strokes at the age of twelve weeks. Rats given tocotrienols between the ages of eight to twelve weeks experienced a reduction in injured brain volume compared to that observed in rats who did not receive tocotrienols. Examination of the brains of the animals who received tocotrienols found a significantly higher level of the vitamin than that measured in the control rats. A second study which supplemented rats with alpha-tocotrienol for a longer period produced similar results.
The authors write that their “findings demonstrate that 12-Lox deficiency protects against stroke injury.” They conclude, “This study demonstrated that oral tocotrienol supplementation may protect against stroke in vivo.”
Most strokes culminate in a core area of cell death (infarction) in which blood flow is so drastically reduced that the cells usually cannot recover. This threshold seems to occur when cerebral blood flow is 20% of normal or less. Brain cells ultimately die as a result of the actions of calcium-activated proteases (enzymes which digest cell proteins), lipases (enzymes which digest cell membranes), and free radicals formed as a result of the ischemic cascade.
Without neuroprotective agents, nerve and brain cells may be irreversibly damaged within several minutes. This knowledge is leading to unprecedented therapy development. Expanding knowledge regarding the nature of ischemic brain cell injury is leading researchers to focus on the development of calcium antagonists, glutamate antagonists, antioxidants, and other types of neuroprotective agents.
An analysis of 18 trials documented a 23% reduction in stroke risk with anti-platelet agents. The drug ticlopidine was found to be the most effective anti-platelet agent, but its adverse side effects frequently restrict its long-term use. A more benign approach such as use of aspirin or nutrients like ginkgo biloba, melatonin, fish oil, and garlic, as well as green tea extract, may be as effective and are free of side effects.
Tocotrienols have shown superior action in maintaining arterial health. This wonder nutrient is so effective because of its structure of double bonds in the isoprenoid side chain, making it a great scavenger of free radicals.
Sesame lignans have been added to help block or inhibit the enzyme that breaks down tocotrienols allowing tissue levels of tocotrienols to build up in the body. This translates into much greater antioxidant protection, decreasing destructive free radicals.
Protecting brain health is vital if the pursuit of a longer life is to have any meaning. According to current wisdom, some degree of cognitive impairment is all but inevitable as we age. That is, unless steps are taken to prevent it.
Scientists in Texas recently noted, “As life expectancy increases worldwide, pandemics of cognitive impairment and dementia are emerging as major public health problems.” Another research team tried to inject humor into this sobering topic:
“Cognitive aspects of aging represent a grave challenge for our societal circumstances as members of the baby-boom generation spiral toward a collective ‘senior moment.’”
The encouraging news is that scientists have discovered methods to preserve and even restore neurological structure and function. These powerful weapons give aging adults unprecedented control over their cognitive health.
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