Selenium, Memory And Cognitive Function

Research have established linkage between selenium and cognitive function. Selenium deficiency associated with aging increases the risk of cognitive impairment. Selenium is a trace element that is essential for the human body. Selenoproteins are selenium containing protein whose biological function require the presence of selenium. Selenium attach to the protein via amino acid cysteine. Among the group of selenoproteins identified, glutathione peroxidase, thioredoxin reductases and iodothyronine deiodinases are the most thoroughly characterized selenoproteins.  Glutathione peroxidase and thioredoxin reductases belong to the class of antioxidant enzymes which are involved in the redox reaction and are part of the body’s natural defense system for neutralizing free radicals and reactive oxygen species. Free radical is one of the main causes of aging. They are super reactive oxidizing agent, they oxidize other molecules including macromolecules important for biological processes. When protein , DNA and cellular membrane and intracellular organelles are damaged by reactive oxygen species (free radicals), essential biological processes are disrupted and cellular structure are damaged. Selenoproteins glutathione peroxidase, thioredoxin reductases and iodothyronine deiodinases protect brain (and human body ) from free radical damage.

Cognitive function declines naturally with age. Studies have shown that selenium supplementation slows this aging process. Brain oxidative stress is one of the causal factors in brain aging. Not only antioxidant selenoproteins clear free radicals in the brain. Selenium in the brain can also remove beta-amyloid plaque. Beta-amyloid is neurotoxic. Amyloid is fragment of a protein called amyloid precursor. In healthy brain, beta-amyloid do not accumulate – that they are degraded and eliminated.  However, increased beta-amyloid plaque were detected in the Alzheimer’s brain. It accumulates in the nerve cell and ultimately initiates the disease of the brain neuron. Researchers have found that beta-amyloid oligomers induce some of the symptoms of Alzheimer’s disease by competing with insulin for insulin receptor, thus impairing glucose (energy) metabolism in the brain. Research suggests that selenium is able to limit beta-amyloid production in the brain including hippocampus – the region of the brain that is important for long term memory (explicit memory) formation. Dietary selenium deficiency was correlated with elevated level of beta-amyloid plaque in the brain neurons.

Another function of selenium is its detoxifying chelating property that it can bind to toxic heavy metals (e.g.. mercury). This property improves general brain health and protect brain form environmental pollutants and toxic chemicals.

The brain is the organ that the selenium depletion occurs last. Whenever selenium level decreases, the brain is the last place that selenium levels drop, suggesting its importance in the brain. Several longitudinal clinical studies revealed that selenium status (measured by the plasma selenium level) decreases with age and this decrease correlates with the extent of cognitive impairments. More evidence comes from studies for elderlies who live in the geographical regions where the soil is deficient in  selenium and the people living in the region were subject to long-term selenium deficiency. Results from these studies suggest that a long-term chronic deficiency in selenium is associated with increased risk and incidence of cognitive impairments.

Evidence from some medications that have the side effect of inhibiting the activity of selenoproteins also point to the role of selenium in maintaining cognitive health. One such drug is statin which is used to lower cholesterol level and prevent cardiovascular diseases. It was observed that statin users were showing 100% cognitive decline.

Optimal levels of selenium can be maintained via dietary supplements or through diet. The recommended dietary allowances (RDA) is 55 mcg. Optimal level can be 100-200 mcg as long as the supplementation do not exceed 400 mcg. Plasma selenium level can be used as the reference for optimal level determination of supplementation. Over dose of selenium can cause selenosis (see post “Selenium, Selenoproteins And Health”).

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