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© 2004 The American Society for Nutritional Sciences J. Nutr. 134:707-710, April 2004


Recent Advances in Nutritional Sciences

The Neurobiology of Selenium: Lessons from Transgenic Mice1,2

Ulrich Schweizer*,{dagger},3, Lutz Schomburg{dagger} and Nicolai E. Savaskan**

* Neurobiology of Selenium, Neuroscience Research Center; {dagger} Institute for Experimental Endocrinology; and ** Institute of Cell Biology and Neurobiology, Center for Anatomy, Charité University Medical School Berlin, Germany

3To whom correspondence should be addressed. E-mail: ulrich.schweizer{at}charite.de.

The brain represents a privileged organ with respect to selenium (Se) supply and retention. It contains high amounts of this essential trace element, which is efficiently retained even in conditions of Se deficiency. Accordingly, no severe neurological phenotype has been reported for animals exposed to Se-depleted diets. They are, however, more susceptible to neuropathological challenges. Recently, gene disruption experiments supported a pivotal role for different selenoproteins in brain function. Using these and other transgenic models, longstanding questions concerning the preferential supply of Se to the brain and the hierarchy among the different selenoproteins are readdressed. Given that genes for at least 25 selenoproteins have been identified in the human genome, and most of these are expressed in the brain, their specific roles for normal brain function and neurological diseases remain to be elucidated.


KEY WORDS: • selenoprotein P • glutathione peroxidase • tRNASec • MsrB • thioredoxin reductase




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