Author(s): Lucy Elisabeth James and Ayodeji A Asuni
Accrued evidence suggesting that hypovitaminosis D acts as a risk factor for developing Parkinson’s disease (PD) remains controversial. Herein we evaluated existing results, and outline several biological mechanisms by which the hypovitaminosis D-PD relationship may occur. We performed a meta-analysis, using data obtained from a search of PubMed from July 2002 to July 2012, for studies reporting serum vitamin D levels in PD and control patients.We found that in comparison to healthy individuals, those with PD had lower levels of serum vitamin D. Furthermore, we explore a number of potential associated biological mechanisms, including the actions of reactive nitrogen species (RNS), glutathione (GSH), and glial-derived neurotrophic factor (GDNF) in the brain. We also examine the roles of Nurr1 and VDR genes in PD. Although a unifying hypothesis remains challenging, there is evidence to demonstrate that supplementation with the vitamin can to have a positive effect on PD pathobiology. We surmise that hypovitaminosis D does act as a risk factor in the development of PD. However, the need for new epidemiological studies and further research around vitamin D metabolism is highlighted. Urgent efforts to correct vitamin D deficiency through supplementation are warranted as they may improve either motor and/or non-motor symptoms in PD.
