by Emily Mason
Mice retain a high concentration of selenium in the brain despite low levels of this essential element throughout the rest of the body, indicating that the brain is a privileged site for selenium retention.
Interactions between the selenium-rich protein Sepp1 and the apolipoprotein E receptor 2 (apoER2), which facilitates Sepp1 uptake by the brain, may be responsible, Raymond Burk, M.D., and colleagues report in the August FASEB Journal.
These interactions occur at the blood-brain barrier and within the brain to supply neurons with selenium even when dietary levels are low. In mice with mild selenium deficiency, genetic deletion of either protein depressed brain selenium levels and led to severe neurodegeneration. In contrast, mice with intact Sepp1 and apoER2 had only mild neurological dysfunction even when selenium levels were extremely low.
The findings suggest that both proteins are necessary to maintain brain selenium and brain neuron viability under selenium-deficient conditions. By studying selenium metabolism in the brain, neurodegenerative disorders may be better understood.
The study was supported by National Institutes of Health grants ES002497, DK058404 and ES000267.
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