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Parkinson's Disease associations with Vitamin D Receptor and GC gene – June 2016

GC and VDR SNPs and Vitamin D Levels in Parkinson's Disease: The Relevance to Clinical Features.

Neuromolecular Med. 2016 Jun 9.
Gezen-Ak D1, Alaylıoğlu M2, Genç G3, Gündüz A4, Candaş E2, Bilgiç B5, Atasoy İL2, Apaydın H4, Kızıltan G4, Gürvit H5, Hanağası H5, Ertan S4, Yılmazer S2, Dursun E6.

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The items in both Parkinson's Disease and Vitamin D Binding Protein categories are listed here:

The items in both Parkinson's Disease and Vitamin D Receptor categories are listed here:

Overview Parkinson's and Vitamin D contains the following summary

Many genes are NOT noticed by Vitamin D measurements
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1Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, 34098, Istanbul, Turkey. duygugezenak at gmail.com.
2Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, 34098, Istanbul, Turkey.
3Department of Neurology, Gumussuyu Military Hospital, Istanbul, Turkey.
4Department of Neurology, Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey.
5Behavioral Neurology and Movement Disorders Unit, Department of Neurology, Istanbul Faculty of Medicine, Istanbul University, Istanbul, Turkey.
6Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, 34098, Istanbul, Turkey. erdincdu at yahoo.com.

Vitamin D deficiency is suggested to be associated with Parkinson's disease (PD). Our aim was to investigate the serum 25-hydroxyvitamin D3 (25OHD) levels of PD patients in Turkish cohort, to investigate any association of vitamin D binding protein (GC) genotypes with PD due to the significant role of GC in vitamin D transport, to determine whether vitamin D receptor (VDR) haplotype that we previously demonstrated to be a risk haplotype for AD is also a common haplotype for PD and to investigate any relevant consequence of serum 25OHD levels, GC or VDR genotypes on clinical features of PD.

Three hundred eighty-two PD patients and 242 healthy subjects were included in this study. The serum 25OHD levels were investigated by CLIA, and GC and VDR SNPs were evaluated with LightSnip. Our results indicated a strong relationship between low serum 25OHD levels and PD (p < 0.001). rs7041 of GC and ApaI of VDR were associated with the PD risk (p < 0.05).

Minor allele carriers for BsmI of VDR gene in both PD patients and healthy subjects had significantly higher levels of serum 25OHD (p < 0.05).

The homozygous major allele carriers for rs2282679, rs3755967 and rs2298850 of GC gene in PD patients with slower progression had significantly higher levels of serum 25OHD (p < 0.05).

Minor allele carriers for FokI of VDR gene were more frequent in patients with advanced-stage PD (p < 0.05). Consequently, this is the first study demonstrating GC gene as a risk factor for PD. The relationship between PD's clinical features and low 25OHD or risk genotypes might have effects on PD independently.

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