Cerebral small vessel disease 2.5 X more likely if poor Vitamin D Receptor

Created June 2018

Vitamin D receptor (VDR) gene polymorphism and vascular dementia due to cerebral small vessel disease in an Asian Indian cohort

Journal of the Neurological Sciences https://doi.org/10.1016/j.jns.2018.05.025

Manjunath Supriyaa Sadanandavalli Retnaswami Chandrab Puttachandra Prabhakara Chandrajit Prasadc Rita Christophera

From Cerebral Small Vessel Disease: What to Know & What to Do 2018?It appears that cerebral small vessel disease can increase* White portions of MRI (poor blood flow) aka White matter hyperintensities* Note: Multiple Sclerosis shows up as increased white matter on MRIs* Cognitive decline* Problems with walking or balance* Strokes* Vascular dementia.---Note: Poor Vitamin D Receptors result in less Vitamin D getting to cells,     but DOES NOT reduce the Vitamin D levels in the bloodItems in both categories Cognition and Vitamin D Receptor are listed here: {category}Items in both categories Stroke and Vitamin D Receptor are listed here: {category}Items in both categories Parkinson's and Vitamin D Receptor are listed here: {category}---Vitamin D Receptor category has the following{include}

Highlights

  • Vitamin D acting through VDR plays a crucial role in vascular health.

  • VDR FokI “f” allele increases risk of cerebral SVD by 1.5-fold in men.

  • Serum vitamin D is significantly lower in subjects with FokI “ff” genotype.

  • FokI “ff” increases risk of SVD by 2.5-fold in subjects with low serum vitamin D

  • ApaI polymorphism confers protection against SVD in women.

Vitamin D receptor (VDR) and its ligand Vitamin D, play a crucial role in regulating multiple pathways for maintaining vascular health. The present study aimed at evaluating whether single nucleotide polymorphisms in VDR gene were associated with susceptibility to vascular dementia (VaD) due to cerebral small vessel disease (SVD). A total of 644 subjects (302 patients diagnosed with cerebral SVD-associated VaD and 342, age- and gender-matched healthy controls) were genotyped for VDR gene variants, FokI, ApaI, TaqI and BsmI, by PCR-RFLP method. Among the 4 examined VDR variants, the presence of the minor allele (Ff+ff vs FF) of FokI variant increased the risk for cerebral SVD by 1.5-fold in men (p = 0.047). Serum 25-hydroxyvitamin D [25(OH)D] was lower in subjects having the FokI “ff” genotype compared to those with the “FF” genotype (p = 0.044). Moreover, in subjects with low serum 25(OH)D the presence of “ff” genotype increased the odds of SVD by 2.5 folds (p = 0.041). ApaI polymorphism decreased the risk of cerebral SVD in women. The distribution of TaqI and BsmI variants were not significantly different between patients and controls. Further studies in large cohorts are necessary to validate the role of FokI polymorphism in cerebral SVD and VaD etiopathogenesis.

Tags: Cognitive Stroke Vit D Receptor