Parkinson’s Disease, low vitamin D and Vit. D genetics
Vitamin D deficiency and genetic polymorphisms of Vitamin D-associated genes in Parkinson’s Disease
European Journal of Neuroscience preprint DOI: 10.22541/au.167407862.25881100/v1
Barnali Ray Basu1, Randrita Pal1, Supriyo Choudhury2, Hrishikesh Kumar2, Sanjit Dey3, and Nilansu Das1
1Surendranath College
2Institute of Neurosciences Kolkata
3University of Calcutta Faculty Council for Post-Graduate Studies in Science
Parkinson’s Disease (PD) and vitamin D share a unique link as Vitamin D deficiency (VDD) prevails in PD. Thus, an in-depth understanding of Vitamin D biology in PD might be crucial for therapeutic strategies emphasizing Vitamin D. Specifically, explicating the effect of VDD and genetic polymorphisms of vitamin D-associated genes in PD, like
VDR (Vitamin D Receptor) or
GC (Vitamin D Binding Protein),
may aid the process along with polymorphisms of Vitamin D metabolizing genes (e.g., CYP2R1, CYP27A1 ) in PD. Literature review of single nucleotide polymorphisms (SNPs) related to Vitamin D levels [GC (GC1- rs7041, GC2-rs4588), CYP2R1, CYP24A1, CYP27B1] and Vitamin D function [VDR (FokI - rs2228570, Apal - rs7976091, BsmI-rs1544410, TaqI-rs731236)] was conducted to explore their relationship with PD severity globally. Furthermore, the DisGeNET database was utilized to explore the gene-disease associations in PD, and STRING alongside Cytoscape was utilized to identify critical genes associated with PD. VDR-FokI polymorphism was reported to be significantly associated with PD in Hungarian, Chinese, and Japanese populations, whereas VDR-ApaI polymorphism was found to affect PD in the Iranian population.
However, VDR-TaqI and BsmI polymorphisms had no significant association with PD severity.
Conversely, GC1 polymorphisms reportedly affected Vitamin D levels without influencing the disease severity.
CYP2R1 (excluding rs1993116) was also reportedly linked to clinical manifestations of PD.
Genetic polymorphisms might cause VDD despite enough sunlight exposure and vitamin D-rich food intake, enhancing inflammation, and thereby influencing PD pathophysiology.
Knowledge of the polymorphisms associated with vitamin D appears promising for developing new therapeutic strategies against PD.
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