Vitamin D deficiency and genetic polymorphisms of vitamin D‐associated genes in Parkinson's disease.
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| Title: | Vitamin D deficiency and genetic polymorphisms of vitamin D‐associated genes in Parkinson's disease. |
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| Authors: | Pal, Randrita (AUTHOR), Choudhury, Supriyo (AUTHOR), Kumar, Hrishikesh (AUTHOR), Dey, Sanjit (AUTHOR), Das, Nilansu (AUTHOR), Basu, Barnali Ray (AUTHOR) |
| Source: | European Journal of Neuroscience. Sep2023, Vol. 58 Issue 5, p3362-3377. 16p. 3 Diagrams, 4 Charts. |
| Subjects: | Vitamin D deficiency, Parkinson's disease, Genetic polymorphisms, Vitamin D receptors, Vitamin D, Single nucleotide polymorphisms |
| Abstract: | 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 emphasising 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 metabolising genes (e.g., CYP2R1 and CYP27A1) in PD. Literature review of single nucleotide polymorphisms (SNPs) related to vitamin D levels [GC (GC1‐rs7041 and GC2‐rs4588), CYP2R1, CYP24A1 and CYP27B1] and vitamin D function [VDR (FokI ‐ rs2228570 and rs10735810; ApaI ‐ rs7976091, rs7975232BsmI and rs1544410; and TaqI ‐ rs731236)] was conducted to explore their relationship with PD severity globally. 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, there by influencing PD pathophysiology. Knowledge of the polymorphisms associated with VDD appears promising for developing precision vitamin D‐dosing therapeutic strategies against PD. [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | 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 emphasising 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 metabolising genes (e.g., CYP2R1 and CYP27A1) in PD. Literature review of single nucleotide polymorphisms (SNPs) related to vitamin D levels [GC (GC1‐rs7041 and GC2‐rs4588), CYP2R1, CYP24A1 and CYP27B1] and vitamin D function [VDR (FokI ‐ rs2228570 and rs10735810; ApaI ‐ rs7976091, rs7975232BsmI and rs1544410; and TaqI ‐ rs731236)] was conducted to explore their relationship with PD severity globally. 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, there by influencing PD pathophysiology. Knowledge of the polymorphisms associated with VDD appears promising for developing precision vitamin D‐dosing therapeutic strategies against PD. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 0953816X |
| DOI: | 10.1111/ejn.16098 |
