Prioritized brain selenium retention and selenoprotein expression: Nutritional insights into Parkinson's disease

Xiong Zhang; Rong-Pei Liu; Wen-Hsing Cheng; Jian-Hong Zhu

doi:10.1016/j.mad.2019.04.004

Prioritized brain selenium retention and selenoprotein expression: Nutritional insights into Parkinson's disease

Mech Ageing Dev. 2019 Jun:180:89-96. doi: 10.1016/j.mad.2019.04.004. Epub 2019 Apr 15.

Authors

Xiong Zhang¹, Rong-Pei Liu², Wen-Hsing Cheng³, Jian-Hong Zhu⁴

Affiliations

¹ Department of Geriatrics and Neurology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
² Department of Geriatrics and Neurology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China; Department of Food Science, Nutrition and Health Promotion, Mississippi State University, Mississippi State, MS, USA.
³ Department of Food Science, Nutrition and Health Promotion, Mississippi State University, Mississippi State, MS, USA. Electronic address: wcheng@fsnhp.msstate.edu.
⁴ Department of Geriatrics and Neurology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China; Department of Preventive Medicine, School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang, China. Electronic address: jhzhu@wmu.edu.cn.

PMID: 30998939
DOI: 10.1016/j.mad.2019.04.004

Abstract

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.

Keywords: Oxidative stress; Parkinson’s disease; Selenium; Selenoprotein.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Animals
Disease Models, Animal
Gene Expression Regulation*
Humans
Mice
Oxidative Stress*
Parkinson Disease / diet therapy
Parkinson Disease / metabolism*
Parkinson Disease / pathology
Selenium / metabolism*
Selenoproteins / biosynthesis*

Substances

Selenoproteins
Selenium