Selenium (34Se), an antioxidant trace element, is an important regulator of brain function.
These beneficial properties that Se possesses are attributed to its ability to be incorporated into
selenoproteins as an amino acid. Several selenoproteins are expressed in the brain, in which some of
them, e.g. glutathione peroxidases (GPxs), thioredoxin reductases (TrxRs) or selenoprotein P (SelP),
are strongly involved in antioxidant defence and in maintaining intercellular reducing conditions.
Since increased oxidative stress has been implicated in neurological disorders, including Parkinson’s
disease, Alzheimer’s disease, stroke, epilepsy and others, a growing body of evidence suggests that Se
depletion followed by decreased activity of Se-dependent enzymes may be important factors
connected with those pathologies. Undoubtedly, the remarkable progress that has been made in
understanding the biological function of Se in the brain has opened up new potential possibilities for
the treatment of neurological diseases by using Se as a potential drug. However, further research in the search for optimal
Se donors is necessary in order to achieve an effective and safe therapeutic income.