Prioritized Brain Selenium Retention and Selenoprotein Expression: Nutritional Insights into Parkinson’s Disease
Xiong Zhang1, Rong-Pei Liu1,2, Wen-Hsing Cheng2 and Jian-Hong Zhu1,3
Selenium (Se), an essential trace mineral, confers its physiological functions mainly through selenoproteins, most of which are oxidoreductases. Results from animal, epidemiological, and human genetic studies link Parkinson’s disease to Se and certain selenoproteins. Parkinson’s disease is characterized by multiple motor and non-motor symptoms that are difficult to diagnose at early stages of the pathogenesis. While irreversible, degenerative and age-related, the onset of Parkinson’s disease may be delayed through proper dietary and environmental controls. One particular attribute of Se biology is that brain has the highest priority to receive and retain this nutrient even in Se deficiency. Thus, brain Se deficiency is rare; however, a strong body of recent evidence implicates selenoprotein dysfunction in Parkinson’s disease. Direct and indirect evidence from mouse models implicate selenoprotein T, glutathione peroxidase 1, selenoprotein P and glutathione peroxidase 4 in counteracting Parkinson’s disease through Se transportation to the brain and reduced oxidative stress. It is of future interest to further characterize the full selenoproteomes in various types of brain cells and elucidate the mechanism of their actions in Parkinson’s disease.